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other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. 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The main objectives of the journal include: providing an intellectual platform for Vietnamese and international scholars; promoting interdisciplinary studies in social sciences and humanities; becoming the leading journal in social sciences and humanities in Vietnam; being indexed by worldwide databases and having academic recognition internationally in the near future.\\nThe journal is currently indexed by Google Scholar, WorldCat, Open Archives, Cosmos Impact Factor, Advanced Sciences Index, Scientific Indexing Services, CrossRef, EBSCO Information Services and Vietnam National University’s digital archive.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Journal of Social Sciences and Humanities-Vietnam\"},{\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"ISSN 2354-1172, email: tapchikhxhnv@gmail.com, tckhxhnv@vnu.edu.vn\"},{\"insert\":\"\\n\"}]}","{\"ops\":[{\"insert\":\"Được thành lập ngày 31\u002F8\u002F2015 (giấy phép hoạt động số 155\u002FGP-BVHTT ngày 11 tháng 5 năm 2015 của Bộ Thông tin và Truyền thông, mã số tiêu chuẩn quốc tế ISSN 2354-1172), Tạp chí Khoa học Xã hội và Nhân văn (Journal of Social Sciences and Humanities) là ấn phẩm khoa học chính thức, duy nhất của Trường Đại học Khoa học Xã hội và Nhân văn, ĐHQG Hà Nội, phát triển và kế thừa Chuyên san Khoa học Xã hội và Nhân văn, Tạp chí Khoa học, ĐHQG Hà Nội.\\nTạp chí xuất bản định kỳ (04 số tiếng Việt\u002Fnăm và 02 số tiếng Anh\u002Fnăm), có nhiệm vụ \"},{\"attributes\":{\"italic\":true},\"insert\":\"công bố, giới thiệu các công trình nghiên cứu khoa học khoa học xã hội và nhân văn của các tác giả là các nhà khoa học trong và ngoài nước, phục vụ giảng dạy, học tập và nghiên cứu khoa học\"},{\"insert\":\". Hội đồng biên tập của Tạp chí hiện bao gồm 33 nhà khoa học có uy tín trong nước và quốc tế. Tạp chí tập trung và ưu tiên đăng tải những bài báo theo định hướng của tinh thần cởi mở, sáng tạo, nhanh chóng vươn lên để tiếp cận và sánh ngang với các tạp chí có uy tín hàng đầu của khu vực và trên thế giới. Nội dung chính của Tạp chí bao gồm các Bài nghiên cứu (khoảng 6000 đến 15000 từ), các bài điểm sách, thông tin khoa học (khoảng 300 đến 1500 từ) được trình bày theo đúng cấu trúc và chuẩn mực của một tạp chí khoa học.\\nCác bài viết của Tạp chí hiện đang được trích dẫn bởi Google Scholar, WorldCat, Open Archives, Cosmos Impact Factor, Advanced Sciences Index, Scientific Indexing Services, CrossRef, EBSCO Information Services.\\nMọi thông tin xin liên hệ: \"},{\"attributes\":{\"italic\":true},\"insert\":\"Phòng Tạp chí, 701 - E, Trường Đại học Khoa học Xã hội và Nhân văn, 336 Nguyễn Trãi, Thanh Xuân, Hà Nội. ĐT: 024.35581984; email: tckhxhnv@vnu.edu.vn \"},{\"insert\":\"hoặc \"},{\"attributes\":{\"italic\":true},\"insert\":\"tapchikhxhnv@gmail.com \"},{\"insert\":\"\\n\"}]}",{"EN":494,"VI":495},"VNU Journal of Social Sciences and Humanities","Tạp chí Khoa học Xã hội và Nhân văn",[101,102],[],[499],{"id":500,"createTime":501,"updateTime":502,"relativeEntities":503,"slug":504,"properties":505,"entityType":98,"verifyStatus":25,"verifyTime":509,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":222,"url":26,"parentIds":510,"statistic":511},"8b6e349b-0daf-4895-9c3f-85f30f1bfd42","2023-07-31T12:55:58.430+00:00","2026-06-19T02:30:07.899+00:00",[],"Tr%C6%B0%E1%BB%9Dng-%C4%90%E1%BA%A1i-h%E1%BB%8Dc-Khoa-h%E1%BB%8Dc-X%C3%A3-h%E1%BB%99i-v%C3%A0-Nh%C3%A2n-v%C4%83n-%C4%90%E1%BA%A1i-h%E1%BB%8Dc-Qu%E1%BB%91c-gia-H%C3%A0-N%E1%BB%99i",{"title":506},{"EN":507,"VI":508},"VNU University of Social Sciences and Humanities","Trường Đại học Khoa học Xã hội và Nhân văn, Đại học Quốc gia Hà Nội","2023-08-02T15:28:49.057+00:00",[],{"impactFactor":36,"impactFactorByYear":512,"i10Index":59,"i10IndexLast5Year":115,"totalPublication":514,"totalPublicationByYear":515,"totalCitation":518,"totalCitationByYear":519,"totalCitationPerPublication":520,"totalCitationPerPublicationByYear":521,"hindexLast5Year":162,"hindex":162},{"2016":229,"2017":230,"2018":229,"2021":230,"2022":58,"2023":513,"2024":38},0.15,365,{"2013":115,"2014":158,"2015":125,"2016":252,"2017":44,"2018":516,"2019":286,"2020":396,"2021":259,"2022":517,"2023":396,"2024":115,"2025":59,"2026":115},21,42,169,{"2015":283,"2016":135,"2017":52,"2018":50,"2019":298,"2020":53,"2021":359,"2022":115,"2023":115},0.46,{"2015":266,"2016":57,"2017":57,"2018":522,"2019":523,"2020":524,"2021":368,"2022":229,"2023":39},0.38,0.32,0.37,[],"http:\u002F\u002Fjournal.ussh.vnu.edu.vn\u002Findex.php\u002Fvjossh","\u002Fapi\u002Fpublic\u002Ffile\u002Fpublisher\u002F2b8d7b12-2d20-4777-be98-077f44f03c69\u002F0bd0751202944a4b4165b482e6e623e4.png",{"impactFactor":36,"impactFactorByYear":529,"i10Index":162,"i10IndexLast5Year":115,"totalPublication":530,"totalPublicationByYear":531,"totalCitation":537,"totalCitationByYear":538,"totalCitationPerPublication":343,"totalCitationPerPublicationByYear":540,"hindexLast5Year":135,"hindex":135},{"2016":341,"2017":39,"2018":229,"2019":38,"2020":110,"2021":231,"2022":231,"2023":341,"2024":39},764,{"2015":255,"2016":245,"2017":532,"2018":259,"2019":533,"2020":534,"2021":535,"2022":536,"2023":534,"2024":254,"2025":50},111,106,68,92,89,265,{"2015":539,"2016":241,"2017":168,"2018":51,"2019":349,"2020":260,"2021":244,"2022":298,"2023":114},46,{"2015":541,"2016":523,"2017":524,"2018":290,"2019":542,"2020":522,"2021":523,"2022":57,"2023":39},1.48,0.63,{"id":544,"createTime":545,"updateTime":546,"relativeEntities":547,"slug":548,"properties":549,"entityType":24,"verifyStatus":25,"verifyTime":26,"verifyNote":558,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":50,"subjectFields":559,"manageAffiliations":560,"indexDatabases":561,"url":562,"thumbnailPath":563,"statistic":564,"gsStatistic":26,"type":26,"analyzePriority":26},"6ec01bd0-15c0-469a-86ac-41339076ae0a","2023-08-10T07:08:33.153+00:00","2026-01-31T21:19:06.362+00:00",[],"T%E1%BA%A1p-ch%C3%AD-Da-li%E1%BB%85u-h%E1%BB%8Dc-Vi%E1%BB%87t-Nam",{"country":550,"issn":551,"introduce":553,"title":555},{"VOID":15},{"VOID":552},"18594824",{"VI":554},"{\"ops\":[{\"insert\":\"Tạp chí “Da liễu học Việt Nam” (Tiếng Anh: Vietnamese Journal of Dermatology and Venereology) thuộc Hội Da liễu Việt Nam, xuất bản 4 số mỗi năm bằng tiếng Việt hoặc tiếng Anh.\\nTạp chí Da liễu học Việt Nam hoạt động với mục đích, tôn chỉ là phổ biến, trao đổi thông tin trong lĩnh vực chuyên ngành da liễu; đăng tải các công trình nghiên cứu khoa học; chuyển giao công nghệ - kinh tế và khoa học kỹ thuật liên quan đến lĩnh vực da liễu.\\nPhạm vi của tạp chí là tất cả các bài báo khoa học, bài tổng quan, giới thiệu ca lâm sàng, … có liên quan tới chuyên ngành da liễu trong và ngoài nước. 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Hội đồng biên tập tạp chí bao gồm các nhà khoa học có uy tín (Giáo sư, Phó Giáo sư, Tiến sĩ, Bác sĩ…) trong chuyên ngành da liễu nhằm đảm bảo chất lượng và tính khách quan, khoa học cho các bài viết đăng trên Tạp chí.\\n\"}]}",{"EN":556,"VI":557},"Vietnamese Journal of Dermatology and Venereology","Tạp chí Da liễu học Việt Nam","Admin Import",[],[],[],"https:\u002F\u002Fvjdv.vn\u002Findex.php\u002Fvjdv","\u002Fapi\u002Fpublic\u002Ffile\u002Fpublisher\u002F6ec01bd0-15c0-469a-86ac-41339076ae0a\u002F3cbc81720e58429dc7b1c4d7ab1935ca.jpg",{"impactFactor":36,"impactFactorByYear":565,"i10Index":36,"i10IndexLast5Year":36,"totalPublication":566,"totalPublicationByYear":567,"totalCitation":116,"totalCitationByYear":570,"totalCitationPerPublication":109,"totalCitationPerPublicationByYear":571,"hindexLast5Year":115,"hindex":115},{"2023":38,"2024":230},182,{"2022":568,"2023":45,"2024":569},69,56,{"2022":52,"2023":115},{"2022":40,"2023":229},{"id":573,"createTime":574,"updateTime":575,"relativeEntities":576,"slug":577,"properties":578,"entityType":24,"verifyStatus":25,"verifyTime":26,"verifyNote":27,"syncStatus":28,"languages":587,"translateLanguages":26,"viewCount":283,"subjectFields":588,"manageAffiliations":589,"indexDatabases":647,"url":648,"thumbnailPath":649,"statistic":650,"gsStatistic":26,"type":26,"analyzePriority":26},"19221551-7519-47ff-a892-331d1139c64b","2023-09-12T07:03:05.744+00:00","2026-01-24T20:54:40.144+00:00",[],"T%E1%BA%A1p-ch%C3%AD-Khoa-h%E1%BB%8Dc-S%E1%BB%A9c-kho%E1%BA%BB-%C4%90%E1%BA%A1i-h%E1%BB%8Dc-Qu%E1%BB%91c-gia-Th%C3%A0nh-ph%E1%BB%91-H%E1%BB%93-Ch%C3%AD-Minh",{"country":579,"issn":580,"introduce":582,"title":584},{"VOID":15},{"VOID":581},"27349446",{"EN":583},"{\"ops\":[{\"attributes\":{\"bold\":true},\"insert\":\"1. 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And the first issue was published in January 1998 with ISSN 1859-0128. Since then, STDJ has become the most important scientific forum of scientists from VNU-HCM as well as other universities. The magazine has undergone 20 years of development and has become a bridge for scientific exchanges, as well as enriching reference materials for the faculty, doctoral students, students of VNU-HCM in particular and other universities, institutes...\"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"insert\":\"Science and Technology Development Journal - Health Sciences (STDJ-HS) is a subjournal of Science and Technology Development Journal since 2020.\"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"insert\":\" \"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"2. 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The caspase cascade responsible for executing cell death following cytochrome\u003Cjats:italic>c\u003C\u002Fjats:italic>release is well described; however the distinct roles of caspases-9, -3 and -7 during this process are not completely defined.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Here we demonstrate several unique functions for each of these caspases during cell death. Specific inhibition of caspase-9 allows for efficient release of cytochrome\u003Cjats:italic>c\u003C\u002Fjats:italic>, but blocks changes in mitochondrial morphology and ROS production. We show that caspase-9 can cleave Bid into tBid at amino acid 59 and that this cleavage of Bid is required for ROS production following serum withdrawal. We also demonstrate that caspase-3-deficient MEFs are less sensitive to intrinsic cell death stimulation, yet have higher ROS production. In contrast, caspase-7-deficient MEFs are not resistance to intrinsic cell death, but remain attached to the ECM.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusions\u003C\u002Fjats:title>\u003Cjats:p>Taken together, these data suggest that caspase-9 is required for mitochondrial morphological changes and ROS production by cleaving and activating Bid into tBid. After activation by caspase-9, caspase-3 inhibits ROS production and is required for efficient execution of apoptosis, while effector caspase-7 is required for apoptotic cell detachment.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\u003Cjats:sec>\u003Cjats:title>Giới thiệu\u003C\u002Fjats:title>\u003Cjats:p>Apoptosis là một hình thức chết tế bào có lập trình được điều hòa bởi gia đình protein Bcl-2 và gia đình protein caspase. Đường truyền caspase chịu trách nhiệm thực hiện cái chết tế bào sau khi giải phóng cytochrome\u003Cjats:italic>c\u003C\u002Fjats:italic> đã được mô tả rõ ràng; tuy nhiên, vai trò khác biệt của các caspase-9, -3 và -7 trong quá trình này vẫn chưa được xác định hoàn toàn.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Kết quả\u003C\u002Fjats:title>\u003Cjats:p>Trong nghiên cứu này, chúng tôi chứng minh một số chức năng độc đáo cho mỗi caspase trong quá trình chết tế bào. Việc ức chế đặc hiệu caspase-9 cho phép giải phóng cytochrome\u003Cjats:italic>c\u003C\u002Fjats:italic> một cách hiệu quả, nhưng ngăn cản sự thay đổi hình thái của ti thể và sản xuất ROS. Chúng tôi cho thấy rằng caspase-9 có thể cắt Bid thành tBid tại axit amin 59 và sự cắt này của Bid là cần thiết cho việc sản xuất ROS sau khi rút serum. Chúng tôi cũng chứng minh rằng các MEFs thiếu caspase-3 ít nhạy cảm hơn với kích thích cái chết tế bào nội tại, nhưng có sản xuất ROS cao hơn. Ngược lại, các MEFs thiếu caspase-7 không kháng lại cái chết tế bào nội tại, nhưng vẫn gắn kết với ECM.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Kết luận\u003C\u002Fjats:title>\u003Cjats:p>Tổng hợp dữ liệu này cho thấy caspase-9 là cần thiết cho sự thay đổi hình thái ti thể và sản xuất ROS qua việc cắt và kích hoạt Bid thành tBid. Sau khi được kích hoạt bởi caspase-9, caspase-3 ức chế sản xuất ROS và là cần thiết cho việc thực hiện apoptosis một cách hiệu quả, trong khi caspase-7 hiệu ứng là cần thiết cho việc tách biệt tế bào apoptotic.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":750,"VI":751},"Caspase-9, caspase-3 and caspase-7 have distinct roles during intrinsic apoptosis","Caspase-9, caspase-3 và caspase-7 có vai trò khác nhau trong quá trình tự chết tế bào",{"VOID":753},"23834359",{"VOID":755},"10.1186\u002F1471-2121-14-32","PUBLICATION","Auto 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USA",{"openalex":778,"title":780},{"VOID":779},"A5031400042",{"EN":781},"Enriqué Cepero",{"id":783,"sortIndex":115,"researcher":26,"roles":784,"affiliations":785,"properties":792},"5c4298d4-0757-451a-b308-db688dccfc0b",[],[786],{"id":787,"sortIndex":36,"affiliation":788,"properties":26},"32edf719-5d48-453b-8fe7-5c3d18e92b94",{"id":769,"createTime":770,"updateTime":771,"relativeEntities":789,"slug":773,"properties":790,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":791},{"VI":776},{"openalex":793,"orcid":795,"title":797},{"VOID":794},"A5058604628",{"VOID":796},"https:\u002F\u002Forcid.org\u002F0000-0002-7473-8396",{"EN":798},"Luis 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USA",{"id":814,"sortIndex":115,"affiliation":815,"properties":26},"ce7fc759-ee62-41fc-90a9-45e658642f6c",{"id":816,"createTime":817,"updateTime":818,"relativeEntities":819,"slug":820,"properties":821,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"ee9d9dcc-469b-4626-80d5-ebc80a6b8fa6","2024-01-04T16:51:39.106+00:00","2024-09-21T22:31:48.736+00:00",[],"Sheila-and-David-Fuente-Graduate-Program-in-Cancer-Biology-University-of-Miami-Miller-School-of-Medicine-Miami-USA",{"title":822},{"VI":823},"Sheila and David Fuente Graduate Program in Cancer Biology, University of Miami Miller School of Medicine, Miami, USA",{"openalex":825,"title":827},{"VOID":826},"A5074284145",{"EN":828},"Matthew 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NN, Korsmeyer SJ: Cell death: critical control points. Cell. 2004, 116 (2): 205-219. 10.1016\u002FS0092-8674(04)00046-7.",{"doi":901},"10.1016\u002FS0092-8674(04)00046-7",{"id":26,"text":903,"url":26,"identifiers":904},"Galluzzi L, Vitale I, Abrams JM, Alnemri ES, Baehrecke EH, Blagosklonny MV, Dawson TM, Dawson VL, El-Deiry WS, Fulda S: Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012. Cell Death Differ. 2012, 19 (1): 107-120. 10.1038\u002Fcdd.2011.96.",{"doi":905},"10.1038\u002Fcdd.2011.96",{"id":26,"text":907,"url":26,"identifiers":908},"Wei MC, Lindsten T, Mootha VK, Weiler S, Gross A, Ashiya M, Thompson CB, Korsmeyer SJ: tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c. Genes Dev. 2000, 14 (16): 2060-2071.",{"doi":909},"10.1101\u002Fgad.14.16.2060",{"id":26,"text":911,"url":26,"identifiers":912},"Eskes R, Desagher S, Antonsson B, Martinou JC: Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane. 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Cell. 1997, 91 (4): 479-489. 10.1016\u002FS0092-8674(00)80434-1.",{"doi":921},"10.1016\u002FS0092-8674(00)80434-1",{"id":26,"text":923,"url":26,"identifiers":924},"Srinivasula SM, Ahmad M, Fernandes-Alnemri T, Alnemri ES: Autoactivation of procaspase-9 by Apaf-1-mediated oligomerization. Mol Cell. 1998, 1 (7): 949-957. 10.1016\u002FS1097-2765(00)80095-7.",{"doi":925},"10.1016\u002FS1097-2765(00)80095-7",{"id":26,"text":927,"url":26,"identifiers":928},"Woo M, Hakem R, Soengas MS, Duncan GS, Shahinian A, Kagi D, Hakem A, McCurrach M, Khoo W, Kaufman SA: Essential contribution of caspase 3\u002FCPP32 to apoptosis and its associated nuclear changes. Genes Dev. 1998, 12 (6): 806-819. 10.1101\u002Fgad.12.6.806.",{"doi":929},"10.1101\u002Fgad.12.6.806",{"id":26,"text":931,"url":26,"identifiers":932},"Shi Y: Mechanisms of caspase activation and inhibition during apoptosis. Mol Cell. 2002, 9 (3): 459-470. 10.1016\u002FS1097-2765(02)00482-3.",{"doi":933},"10.1016\u002FS1097-2765(02)00482-3",{"id":26,"text":935,"url":26,"identifiers":936},"Scorrano L, Ashiya M, Buttle K, Weiler S, Oakes SA, Mannella CA, Korsmeyer SJ: A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis. Dev Cell. 2002, 2 (1): 55-67. 10.1016\u002FS1534-5807(01)00116-2.",{"doi":937},"10.1016\u002FS1534-5807(01)00116-2",{"id":26,"text":939,"url":26,"identifiers":940},"Zamzami N, Susin SA, Marchetti P, Hirsch T, Gomez-Monterrey I, Castedo M, Kroemer G: Mitochondrial control of nuclear apoptosis. J Exp Med. 1996, 183 (4): 1533-1544. 10.1084\u002Fjem.183.4.1533.",{"doi":941},"10.1084\u002Fjem.183.4.1533",{"id":26,"text":943,"url":26,"identifiers":944},"Martin SJ, Green DR: Protease activation during apoptosis: death by a thousand cuts?. Cell. 1995, 82 (3): 349-352. 10.1016\u002F0092-8674(95)90422-0.",{"doi":945},"10.1016\u002F0092-8674(95)90422-0",{"id":26,"text":947,"url":26,"identifiers":948},"Cepero E, King AM, Coffey LM, Perez RG, Boise LH: Caspase-9 and effector caspases have sequential and distinct effects on mitochondria. Oncogene. 2005, 24 (42): 6354-6366.",{"doi":949},"10.1038\u002Fsj.onc.1208793",{"id":26,"text":951,"url":26,"identifiers":952},"Slee EA, Harte MT, Kluck RM, Wolf BB, Casiano CA, Newmeyer DD, Wang HG, Reed JC, Nicholson DW, Alnemri ES: Ordering the cytochrome c-initiated caspase cascade: hierarchical activation of caspases-2, -3, -6, -7, -8, and -10 in a caspase-9-dependent manner. J Cell Biol. 1999, 144 (2): 281-292. 10.1083\u002Fjcb.144.2.281.",{"doi":953},"10.1083\u002Fjcb.144.2.281",{"id":26,"text":955,"url":26,"identifiers":956},"Stennicke HR, Jurgensmeier JM, Shin H, Deveraux Q, Wolf BB, Yang X, Zhou Q, Ellerby HM, Ellerby LM, Bredesen D: Pro-caspase-3 is a major physiologic target of caspase-8. J Biol Chem. 1998, 273 (42): 27084-27090. 10.1074\u002Fjbc.273.42.27084.",{"doi":957},"10.1074\u002Fjbc.273.42.27084",{"id":26,"text":959,"url":26,"identifiers":960},"Thornberry NA, Rano TA, Peterson EP, Rasper DM, Timkey T, Garcia-Calvo M, Houtzager VM, Nordstrom PA, Roy S, Vaillancourt JP: A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis. J Biol Chem. 1997, 272 (29): 17907-17911. 10.1074\u002Fjbc.272.29.17907.",{"doi":961},"10.1074\u002Fjbc.272.29.17907",{"id":26,"text":963,"url":26,"identifiers":964},"Lakhani SA, Masud A, Kuida K, Porter GA, Booth CJ, Mehal WZ, Inayat I, Flavell RA: Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science. 2006, 311 (5762): 847-851. 10.1126\u002Fscience.1115035.",{"doi":965},"10.1126\u002Fscience.1115035",{"id":26,"text":967,"url":26,"identifiers":968},"Walsh JG, Cullen SP, Sheridan C, Luthi AU, Gerner C, Martin SJ: Executioner caspase-3 and caspase-7 are functionally distinct proteases. Proc Natl Acad Sci USA. 2008, 105 (35): 12815-12819. 10.1073\u002Fpnas.0707715105.",{"doi":969},"10.1073\u002Fpnas.0707715105",{"id":26,"text":971,"url":26,"identifiers":972},"Gregory CD, Pound JD: Microenvironmental influences of apoptosis in vivo and in vitro. Apoptosis. 2010, 15 (9): 1029-1049. 10.1007\u002Fs10495-010-0485-9.",{"doi":973},"10.1007\u002Fs10495-010-0485-9",{"id":26,"text":975,"url":26,"identifiers":976},"Johnson BW, Cepero E, Boise LH: Bcl-xL inhibits cytochrome c release but not mitochondrial depolarization during the activation of multiple death pathways by tumor necrosis factor-alpha. J Biol Chem. 2000, 275 (40): 31546-31553.",{"doi":977},"10.1074\u002Fjbc.M001363200",{"id":26,"text":979,"url":26,"identifiers":980},"Saraste M: Oxidative phosphorylation at the fin de siecle. Science. 1999, 283 (5407): 1488-1493. 10.1126\u002Fscience.283.5407.1488.",{"doi":981},"10.1126\u002Fscience.283.5407.1488",{"id":26,"text":983,"url":26,"identifiers":984},"Cai J, Jones DP: Superoxide in apoptosis. Mitochondrial generation triggered by cytochrome c loss. J Biol Chem. 1998, 273 (19): 11401-11404. 10.1074\u002Fjbc.273.19.11401.",{"doi":985},"10.1074\u002Fjbc.273.19.11401",{"id":26,"text":987,"url":26,"identifiers":988},"Wen LP, Fahrni JA, Troie S, Guan JL, Orth K, Rosen GD: Cleavage of focal adhesion kinase by caspases during apoptosis. J Biol Chem. 1997, 272 (41): 26056-26061. 10.1074\u002Fjbc.272.41.26056.",{"doi":989},"10.1074\u002Fjbc.272.41.26056",{"id":26,"text":991,"url":26,"identifiers":992},"Johnson BW, Boise LH: Bcl-2 and caspase inhibition cooperate to inhibit tumor necrosis factor-alpha-induced cell death in a Bcl-2 cleavage-independent fashion. J Biol Chem. 1999, 274 (26): 18552-18558. 10.1074\u002Fjbc.274.26.18552.",{"doi":993},"10.1074\u002Fjbc.274.26.18552",{"id":26,"text":995,"url":26,"identifiers":996},"Swift S, Lorens J, Achacoso P, Nolan GP: Rapid production of retroviruses for efficient gene delivery to mammalian cells using 293T cell-based systems. Curr Protoc Immunol. 2001, Chapter 10: Unit 10 17C-",{},false,{"id":999,"createTime":1000,"updateTime":1001,"relativeEntities":1002,"slug":1003,"properties":1004,"entityType":756,"verifyStatus":25,"verifyTime":1022,"verifyNote":757,"syncStatus":28,"languages":1023,"translateLanguages":1024,"viewCount":36,"primaryUrl":1025,"fullTextUrl":26,"authors":1026,"publicationType":861,"publisherRelationship":1127,"citationCount":1152,"citationInfo":1153,"publishDate":1156,"publishYear":1157,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1158,"isForceReanalyzing":997},"1a414875-2901-42a8-90ef-378291e07299","2024-04-16T11:52:04.380+00:00","2025-02-17T21:08:29.285+00:00",[],"Aging-of-mesenchymal-stem-cell-in-vitro",{"mag":1005,"keywords":1007,"pmc":1008,"openalex":1010,"abstract":1012,"title":1015,"pm":1018,"doi":1020},{"VOID":1006},"1804670053",{"VI":741},{"VOID":1009},"1435883",{"VOID":1011},"W1804670053",{"EN":1013,"VI":1014},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>A hot new topic in medical treatment is the use of mesenchymal stem cells (MSC) in therapy. The low frequency of this subpopulation of stem cells in bone marrow (BM) necessitates their in vitro expansion prior to clinical use. We evaluated the effect of long term culture on the senescence of these cells.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Results\u003C\u002Fjats:title>\n            \u003Cjats:p>The mean long term culture was 118 days and the mean passage number was 9. The average number of PD decreased from 7.7 to 1.2 in the 10th passage. The mean telomere length decreased from 9.19 Kbp to 8.7 kbp in the 9th passage. Differentiation potential dropped from the 6th passage on. The culture's morphological abnormalities were typical of the Hayflick model of cellular aging.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n            \u003Cjats:p>We believe that MSC enter senescence almost undetectably from the moment of in vitro culturing. Simultaneously these cells are losing their stem cell characteristics. Therefore, it is much better to consider them for cell and gene therapy early on.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Thông tin nền\u003C\u002Fjats:title>\n            \u003Cjats:p>Một chủ đề nóng hổi trong điều trị y tế là sử dụng tế bào gốc trung mô (MSC) trong liệu pháp chữa bệnh. Tần suất thấp của phân nhóm tế bào gốc này trong tủy xương (BM) yêu cầu phải mở rộng nuôi cấy in vitro trước khi sử dụng lâm sàng. Chúng tôi đã đánh giá tác động của việc nuôi cấy dài hạn lên sự lão hóa của các tế bào này.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết quả\u003C\u002Fjats:title>\n            \u003Cjats:p>Thời gian nuôi cấy trung bình là 118 ngày và số lần chuyển dạng trung bình là 9. Số lượng PD trung bình giảm từ 7,7 xuống 1,2 ở lần chuyển dạng thứ 10. Độ dài telomere trung bình giảm từ 9,19 Kbp xuống 8,7 Kbp ở lần chuyển dạng thứ 9. Tiềm năng phân hóa giảm từ lần chuyển dạng thứ 6 trở đi. Các bất thường dạng hình của nuôi cấy là điển hình của mô hình lão hóa tế bào Hayflick.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết luận\u003C\u002Fjats:title>\n            \u003Cjats:p>Chúng tôi tin rằng MSC bắt đầu lão hóa gần như không thể phát hiện ngay từ thời điểm nuôi cấy in vitro. Đồng thời, các tế bào này cũng đang mất đi các đặc tính của tế bào gốc. Do đó, việc xem xét chúng cho liệu pháp tế bào và gene sớm là tốt hơn nhiều.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>",{"EN":1016,"VI":1017},"Aging of mesenchymal stem cell in vitro","Lão hóa của tế bào gốc trung mô in vitro",{"VOID":1019},"16529651",{"VOID":1021},"10.1186\u002F1471-2121-7-14","2024-12-28T05:08:09.915+00:00",[102],[101],"https:\u002F\u002Fbmcmolcellbiol.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2121-7-14",[1027,1046,1061,1082,1097,1112],{"id":1028,"sortIndex":115,"researcher":26,"roles":1029,"affiliations":1030,"properties":1041},"aa8acffb-882c-4286-9043-6fcda68c3e45",[],[1031],{"id":1032,"sortIndex":36,"affiliation":1033,"properties":26},"a8528c4c-9636-4bf1-a634-b16b6f694fe2",{"id":1034,"createTime":1035,"updateTime":1035,"relativeEntities":1036,"slug":1037,"properties":1038,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"e63371f1-c5fa-4c77-ad24-8e54a5ad5169","2024-04-16T11:52:04.427+00:00",[],"Hematology-Oncology-BMT-Research-Center-Shariati-Hospital-Tehran-University-of-Medical-Sciences-Iran",{"title":1039},{"EN":1040},"Hematology-Oncology & BMT Research Center, Shariati Hospital, Tehran University of Medical Sciences, Iran",{"openalex":1042,"title":1044},{"VOID":1043},"A5040348288",{"EN":1045},"Kamran Alimoghaddam",{"id":1047,"sortIndex":36,"researcher":26,"roles":1048,"affiliations":1049,"properties":1056},"c0df4aac-6a05-414c-9ac5-92c4b8b692bd",[],[1050],{"id":1051,"sortIndex":36,"affiliation":1052,"properties":26},"c7c0ac7d-88ef-46a7-b32c-2ffa6d24f78d",{"id":1034,"createTime":1035,"updateTime":1035,"relativeEntities":1053,"slug":1037,"properties":1054,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1055},{"EN":1040},{"openalex":1057,"title":1059},{"VOID":1058},"A5068622860",{"EN":1060},"Mandana Mohyeddin Bonab",{"id":1062,"sortIndex":114,"researcher":26,"roles":1063,"affiliations":1064,"properties":1075},"cd8670fa-dea2-40be-b638-2fed2765afd3",[],[1065],{"id":1066,"sortIndex":36,"affiliation":1067,"properties":26},"93cec98d-bf64-4e74-babf-88f92f9d32f1",{"id":1068,"createTime":1069,"updateTime":1069,"relativeEntities":1070,"slug":1071,"properties":1072,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"3bf975e6-1b7e-4ed8-861f-b7fda4cab3d0","2024-04-16T11:52:04.415+00:00",[],"Immunogenetics-lab-Dept-of-Immunology-College-of-Medicine-Tehran-University-of-Medical-Sciences-Tehran-Iran",{"title":1073},{"EN":1074},"Immunogenetics lab, Dept. of Immunology, College of Medicine, Tehran University of Medical Sciences, Tehran, Iran",{"openalex":1076,"orcid":1078,"title":1080},{"VOID":1077},"A5052089034",{"VOID":1079},"https:\u002F\u002Forcid.org\u002F0000-0002-8336-0348",{"EN":1081},"Fatemeh Talebian",{"id":1083,"sortIndex":162,"researcher":26,"roles":1084,"affiliations":1085,"properties":1092},"cfad17ad-5360-4dd3-b167-bd010ae1afb1",[],[1086],{"id":1087,"sortIndex":36,"affiliation":1088,"properties":26},"d603ef27-9f72-4780-a04a-85ae9efb0bf5",{"id":1068,"createTime":1069,"updateTime":1069,"relativeEntities":1089,"slug":1071,"properties":1090,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1091},{"EN":1074},{"openalex":1093,"title":1095},{"VOID":1094},"A5046169719",{"EN":1096},"Behrouz Nikbin",{"id":1098,"sortIndex":59,"researcher":26,"roles":1099,"affiliations":1100,"properties":1107},"67a277a0-6ff3-4e93-8e80-3240e0250a0b",[],[1101],{"id":1102,"sortIndex":36,"affiliation":1103,"properties":26},"768c011f-04b0-448a-aa98-1a1861949db8",{"id":1034,"createTime":1035,"updateTime":1035,"relativeEntities":1104,"slug":1037,"properties":1105,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1106},{"EN":1040},{"openalex":1108,"title":1110},{"VOID":1109},"A5066883249",{"EN":1111},"Seyed H. 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Nat Med. 1999, 5 (3): 262-4. 10.1038\u002F6470.",{"doi":1162},"10.1038\u002F6470",{"id":26,"text":1164,"url":26,"identifiers":1165},"Anklesaria P, Kase K, Glowacki J, Holland CA, Sakakeeny MA, Wright JA, FitzGerald TJ, Lee CY, Greenberger JS: Engraftment of a clonal bone marrow stromal cell line in vivo stimulates hematopoietic recovery from total body irradiation. Proc Natl Acad Sci U S A. 1987, 84 (21): 7681-5.",{"doi":1166},"10.1073\u002Fpnas.84.21.7681",{"id":26,"text":1168,"url":26,"identifiers":1169},"Koc ON, Gerson SL, Cooper BW, Dyhouse SM, Haynesworth SE, Caplan AI, Lazarus HM: Rapid hematopoietic recovery after coinfusion of autologous-blood stem cells and culture-expanded marrow mesenchymal stem cells in advanced breast cancer patients receiving high-dose chemotherapy. J Clin Oncol. 2000, 18 (2): 307-16.",{"doi":1170},"10.1200\u002FJCO.2000.18.2.307",{"id":26,"text":1172,"url":26,"identifiers":1173},"Devine SM, Hoffman R: Role of mesenchymal stem cells in hematopoietic stem cell transplantation. Curr Opin Hematol. 2000, 7 (6): 358-63. 10.1097\u002F00062752-200011000-00007.",{"doi":1174},"10.1097\u002F00062752-200011000-00007",{"id":26,"text":1176,"url":26,"identifiers":1177},"Bruder SP, Kurth AA, Shea M, Hayes WC, Jaiswal N, Kadiyala S: Bone regeneration by implantation of purified, culture-expanded human mesenchymal stem cells. J Orthop Res. 1998, 16 (2): 155-62. 10.1002\u002Fjor.1100160202.",{"doi":1178},"10.1002\u002Fjor.1100160202",{"id":26,"text":1180,"url":26,"identifiers":1181},"Fukuda K, Sakamoto N, Narita T, Saitoh K, Kameda T, Iba H, Yasugi S: Application of efficient and specific gene transfer systems and organ culture techniques for the elucidation of mechanisms of epithelial-mesenchymal interaction in the developing gut. Dev Growth Differ. 2000, 42 (3): 207-11. 10.1046\u002Fj.1440-169x.2000.00503.x.",{"doi":1182},"10.1046\u002Fj.1440-169x.2000.00503.x",{"id":26,"text":1184,"url":26,"identifiers":1185},"Friedenstein AJ, Latzinik NW, Grosheva AG, Gorskaya UF: Marrow microenvironment transfer by heterotopic transplantation of freshly isolated and cultured cells in porous sponges. Exp Hematol. 1982, 10 (2): 217-27.",{},{"id":26,"text":1187,"url":26,"identifiers":1188},"Wexler SA, Donaldson C, Denning-Kendall P, Rice C, Bradley B, Hows JM: Adult bone marrow is a rich source of human mesenchymal 'stem' cells but umbilical cord and mobilized adult blood are not. Br J Haematol. 2003, 121 (2): 368-74. 10.1046\u002Fj.1365-2141.2003.04284.x.",{"doi":1189},"10.1046\u002Fj.1365-2141.2003.04284.x",{"id":26,"text":1191,"url":26,"identifiers":1192},"Cheng FJ, Zou P, Zhong ZD, Guo R, Xiao J: The growth characteristics of mesenchymal stem\u002Fprogenitor cells in human umbilical cord blood. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2003, 11 (6): 565-8.",{},{"id":26,"text":1194,"url":26,"identifiers":1195},"Van Zglinicki T, Saretzki G, Docke W, Lotze C: Mild hyperoxia shortens telomeres and inhibits proliferation: a model for senescence?. Exp Cell Res. 1995, 220: 186-10.1006\u002Fexcr.1995.1305.",{"doi":1196},"10.1006\u002Fexcr.1995.1305",{"id":26,"text":1198,"url":26,"identifiers":1199},"Stenderup K, Justesen J, Clausen C, Kassem M: Aging is associated with decreased maximal life span and accelerated senescence of bone marrow stromal cells. Bone. 2003, 33 (6): 919-26. 10.1016\u002Fj.bone.2003.07.005.",{"doi":1200},"10.1016\u002Fj.bone.2003.07.005",{"id":26,"text":1202,"url":26,"identifiers":1203},"Hayflick L: The limited In Vitro lifetime of human diploid cell strains. Exp Cell Res. 1965, 37: 614-36. 10.1016\u002F0014-4827(65)90211-9.",{"doi":1204},"10.1016\u002F0014-4827(65)90211-9",{"id":26,"text":1206,"url":26,"identifiers":1207},"Colter DC, Class R, DiGirolamo CM, Prockop DJ: Rapid expansion of recycling stem cells in cultures of plastic-adherent cells from human bone marrow. Proc Natl Acad Sci U S A. 97 (7): 3213-8. 10.1073\u002Fpnas.070034097. 2000 Mar 28",{"doi":1208},"10.1073\u002Fpnas.97.7.3213",{"id":26,"text":1210,"url":26,"identifiers":1211},"Smith JR, Lincoln DW: Aging of cells in culture. Int Rev Cytol. 1984, 89: 151-77.",{"doi":1212},"10.1016\u002FS0074-7696(08)61303-0",{"id":26,"text":1214,"url":26,"identifiers":1215},"Allsopp RC, Harley CB: Evidence for a critical telomere length in senescent human fibroblasts. Exp Cell Res. 1995, 219 (1): 130-6. 10.1006\u002Fexcr.1995.1213.",{"doi":1216},"10.1006\u002Fexcr.1995.1213",{"id":26,"text":1218,"url":26,"identifiers":1219},"Kolquist KA, Ellisen LW, Counter CM, Meyerson M, Tan LK, Weinberg RA, Haber DA, Gerald WL: Expression of TERT in early premalignant lesions and a subset of cells in normal tissues. Nat Genet. 1998, 19 (2): 182-6. 10.1038\u002F554.",{"doi":1220},"10.1038\u002F554",{"id":26,"text":1222,"url":26,"identifiers":1223},"Baxter MA, Wynn RF, Jowitt SN, Wraith JE, Fairbairn LJ, Bellantuono I: Study of telomere length reveals rapid aging of human marrow stromal cells following in vitro expansion. Stem Cells. 2004, 22 (5): 675-82. 10.1634\u002Fstemcells.22-5-675.",{"doi":1224},"10.1634\u002Fstemcells.22-5-675",{"id":26,"text":1226,"url":26,"identifiers":1227},"Parsch D, Fellenberg J, Brummendorf TH, Eschlbeck AM, Richter W: Telomere length and telomerase activity during expansion and differentiation of human mesenchymal stem cells and chondrocytes. J Mol Med. 2004, 82 (1): 49-55. 10.1007\u002Fs00109-003-0506-z.",{"doi":1228},"10.1007\u002Fs00109-003-0506-z",{"id":26,"text":1230,"url":26,"identifiers":1231},"Pittenger MF, Mackay AM, Beck SC, Jaiswal RK, Douglas R, Mosca JD, Moorman MA, Simonetti DW, Craig S, Marshak DR: Multilineage potential of adult human mesenchymal stem cells. Science. 284 (5411): 143-7. 10.1126\u002Fscience.284.5411.143. 1999 Apr 2",{"doi":1232},"10.1126\u002Fscience.284.5411.143",{"id":26,"text":1234,"url":26,"identifiers":1235},"Digirolamo CM, Stokes D, Colter D, Phinney DG, Class R, Prockop DJ: Propagation and senescence of human marrow stromal cells in culture: a simple colony-forming assay identifies samples with the greatest potential to propagate and differentiate. Br J Haematol. 1999, 107 (2): 275-81. 10.1046\u002Fj.1365-2141.1999.01715.x.",{"doi":1236},"10.1046\u002Fj.1365-2141.1999.01715.x",{"id":26,"text":1238,"url":26,"identifiers":1239},"Conget PA, Minguell JJ: Phenotypical and functional properties of human bone marrow mesenchymal progenitor cells. J Cell Physiol. 1999, 181 (1): 67-73. 10.1002\u002F(SICI)1097-4652(199910)181:1\u003C67::AID-JCP7>3.0.CO;2-C.",{"doi":1240},"10.1002\u002F(SICI)1097-4652(199910)181:1\u003C67::AID-JCP7>3.0.CO;2-C",{"id":26,"text":1242,"url":26,"identifiers":1243},"Rubio D: Spontaneous human adult stem cell transformation. Cancer Res. 65 (8): 3035-9. 2005 Apr 15",{"doi":1244},"10.1158\u002F0008-5472.CAN-04-4194",{"id":26,"text":1246,"url":26,"identifiers":1247},"Serakinci N: Adult human mesenchymal stem cell as a target for neoplastic transformation. Oncogene. 23 (29): 5095-8. 10.1038\u002Fsj.onc.1207651. 2004 Jun 24",{"doi":1248},"10.1038\u002Fsj.onc.1207651",{"id":1250,"createTime":1251,"updateTime":1252,"relativeEntities":1253,"slug":1254,"properties":1255,"entityType":756,"verifyStatus":25,"verifyTime":1273,"verifyNote":757,"syncStatus":28,"languages":1274,"translateLanguages":1275,"viewCount":36,"primaryUrl":1276,"fullTextUrl":26,"authors":1277,"publicationType":861,"publisherRelationship":1368,"citationCount":361,"citationInfo":1389,"publishDate":1391,"publishYear":1392,"citationAnalyzeStatus":1393,"lastCitationAnalyze":1394,"indexDatabases":26,"openAccess":26,"references":1395,"isForceReanalyzing":997},"3e4ebce9-48fc-4815-abc4-de4d4e89d7e1","2024-04-11T17:45:43.144+00:00","2025-02-17T21:10:32.904+00:00",[],"Live-cell-imaging-with-protein-domains-capable-of-recognizing-phosphatidylinositol-4-5-bisphosphate-a-comparative-study",{"mag":1256,"keywords":1258,"pmc":1259,"openalex":1261,"abstract":1263,"title":1266,"pm":1269,"doi":1271},{"VOID":1257},"2078832413",{"VI":741},{"VOID":1260},"2755470",{"VOID":1262},"W2078832413",{"EN":1264,"VI":1265},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>Phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>] is a critically important regulatory phospholipid found in the plasma membrane of all eukaryotic cells. In addition to being a precursor of important second messengers, PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> also regulates ion channels and transporters and serves the endocytic machinery by recruiting clathrin adaptor proteins. Visualization of the localization and dynamic changes in PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> levels in living cells is critical to understanding the biology of PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>. This has been mostly achieved with the use of the pleckstrin homology (PH) domain of PLCδ1 fused to GFP. Here we report on a comparative analysis of several recently-described yeast PH domains as well as the mammalian Tubby domain to evaluate their usefulness as PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> imaging tools.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Results\u003C\u002Fjats:title>\n            \u003Cjats:p>All of the yeast PH domains that have been previously shown to bind PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> showed plasma membrane localization but only a subset responded to manipulations of plasma membrane PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>. None of these domains showed any advantage over the PLCδ1PH-GFP reporter and were compromised either in their expression levels, nuclear localization or by causing peculiar membrane structures. In contrast, the Tubby domain showed high membrane localization consistent with PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> binding and displayed no affinity for the soluble headgroup, Ins(1,4,5)P\u003Cjats:sub>3\u003C\u002Fjats:sub>. Detailed comparison of the Tubby and PLCδ1PH domains showed that the Tubby domain has a higher affinity for membrane PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> and therefore displays a lower sensitivity to report on changes of this lipid during phospholipase C activation.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n            \u003Cjats:p>These results showed that both the PLCδ1PH-GFP and the GFP-Tubby domain are useful reporters of PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> changes in the plasma membrane, with distinct advantages and disadvantages. While the PLCδ1PH-GFP is a more sensitive reporter, its Ins(1,4,5)P\u003Cjats:sub>3\u003C\u002Fjats:sub> binding may compromise its accuracy to measure PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>changes. The Tubby domain is more accurate to report on PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> but its higher affinity and lower sensitivity may limit its utility when phospholipase C activation is only moderate. These studies also demonstrated that similar changes in PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> levels in the plasma membrane can differentially regulate multiple effectors if they display different affinities to PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Nền tảng\u003C\u002Fjats:title>\n            \u003Cjats:p>Phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>] là một phospholipid điều tiết hết sức quan trọng được tìm thấy trong màng plasma của tất cả các tế bào eukaryota. Ngoài việc là tiền chất của các thông điệp thứ cấp quan trọng, PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> còn điều tiết các kênh ion và các transporter, đồng thời phục vụ cho cơ chế nội bào bằng cách tuyển dụng các protein thích hợp clathrin. Việc hình ảnh hóa sự định vị và những thay đổi động lực học trong mức độ PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> trong tế bào sống là rất quan trọng để hiểu biết về sinh học của PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>. Điều này chủ yếu đã được thực hiện bằng cách sử dụng miền pleckstrin homology (PH) của PLCδ1 nối với GFP. Tại đây, chúng tôi báo cáo một phân tích so sánh giữa một số miền PH nấm men được mô tả gần đây cũng như miền Tubby ở động vật có vú để đánh giá tính hữu dụng của chúng như các công cụ hình ảnh PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết quả\u003C\u002Fjats:title>\n            \u003Cjats:p>Tất cả các miền PH nấm men trước đây đã được chỉ ra là liên kết với PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> đều cho thấy sự định vị ở màng plasma nhưng chỉ một phần nhỏ phản ứng với các thao tác điều chỉnh PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> ở màng plasma. Không có miền nào trong số này thể hiện bất kỳ lợi thế nào so với reporter PLCδ1PH-GFP và đều bị ảnh hưởng bởi mức độ biểu hiện, định vị hạt nhân hoặc gây ra các cấu trúc màng đặc biệt. Ngược lại, miền Tubby cho thấy sự định vị ở màng cao, nhất quán với việc liên kết PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> và không hiển thị ái lực với headgroup hòa tan, Ins(1,4,5)P\u003Cjats:sub>3\u003C\u002Fjats:sub>. So sánh chi tiết giữa miền Tubby và PLCδ1PH cho thấy miền Tubby có ái lực cao hơn đối với PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> màng và do đó thể hiện độ nhạy thấp hơn để báo cáo về những thay đổi của lipid này trong quá trình kích hoạt phospholipase C.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết luận\u003C\u002Fjats:title>\n            \u003Cjats:p>Các kết quả này cho thấy rằng cả PLCδ1PH-GFP và miền GFP-Tubby đều là các báo cáo hữu ích về những thay đổi của PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> ở màng plasma, với những lợi thế và nhược điểm rõ ràng. Trong khi PLCδ1PH-GFP là một báo cáo nhạy hơn, việc liên kết với Ins(1,4,5)P\u003Cjats:sub>3\u003C\u002Fjats:sub> của nó có thể làm giảm độ chính xác trong việc đo lường những thay đổi của PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>. Miền Tubby thì chính xác hơn để báo cáo về PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> nhưng ái lực cao hơn và độ nhạy thấp hơn có thể hạn chế tính hữu dụng của nó khi kích hoạt phospholipase C chỉ ở mức vừa phải. Những nghiên cứu này cũng đã chứng minh rằng những thay đổi tương tự trong mức độ PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub> ở màng plasma có thể điều chỉnh khác nhau nhiều hiệu ứng nếu chúng thể hiện các ái lực khác nhau với PtdIns(4,5)\u003Cjats:italic>P\u003C\u002Fjats:italic>\n              \u003Cjats:sub>2\u003C\u002Fjats:sub>.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>",{"EN":1267,"VI":1268},"Live cell imaging with protein domains capable of recognizing phosphatidylinositol 4,5-bisphosphate; a comparative study","Hình ảnh tế bào sống với các miền protein có khả năng nhận biết phosphatidylinositol 4,5-bisphosphate; một nghiên cứu so sánh",{"VOID":1270},"19769794",{"VOID":1272},"10.1186\u002F1471-2121-10-67","2025-02-11T07:44:04.310+00:00",[102],[101],"https:\u002F\u002Fbmcmolcellbiol.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2121-10-67",[1278,1299,1317,1331,1347],{"id":1279,"sortIndex":59,"researcher":26,"roles":1280,"affiliations":1281,"properties":1292},"a31f78c5-49e1-4325-8e11-aff0b98d2cc5",[],[1282],{"id":26,"sortIndex":36,"affiliation":1283,"properties":26},{"id":1284,"createTime":1285,"updateTime":1286,"relativeEntities":1287,"slug":1288,"properties":1289,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"56f937d2-bf4d-4180-b19f-728e0b639d46","2023-12-18T12:55:44.111+00:00","2024-10-13T10:23:24.052+00:00",[],"Department-of-Biochemistry-and-Biophysics-School-of-Medicine-University-of-Pennsylvania-Philadelphia-PA-19104-USA",{"title":1290},{"VI":1291},"Department of Biochemistry and Biophysics, School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA",{"openalex":1293,"orcid":1295,"title":1297},{"VOID":1294},"A5073959537",{"VOID":1296},"https:\u002F\u002Forcid.org\u002F0000-0002-3379-5319",{"EN":1298},"Mark A. Lemmon",{"id":1300,"sortIndex":114,"researcher":26,"roles":1301,"affiliations":1302,"properties":1312},"fcff4181-1305-4244-b448-45d1eed23a45",[],[1303],{"id":26,"sortIndex":36,"affiliation":1304,"properties":26},{"id":1305,"createTime":1306,"updateTime":1306,"relativeEntities":1307,"slug":1308,"properties":1309,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"5f99d0b7-7f5a-493d-b280-75cb0f6bd2cd","2024-04-11T17:45:43.194+00:00",[],"Sections-on-Molecular-Signal-Transduction-Program-for-Developmental-Neuroscience-NICHD-National-Institutes-of-Health-Bethesda-MD-20892-USA",{"title":1310},{"EN":1311},"Sections on Molecular Signal Transduction, Program for Developmental Neuroscience, NICHD, National Institutes of Health, Bethesda, MD, 20892, USA",{"openalex":1313,"title":1315},{"VOID":1314},"A5021531343",{"EN":1316},"Yeun Ju Kim",{"id":1318,"sortIndex":36,"researcher":26,"roles":1319,"affiliations":1320,"properties":1326},"3bd2e273-b388-4794-bce2-810c94e16cd5",[],[1321],{"id":26,"sortIndex":36,"affiliation":1322,"properties":26},{"id":1305,"createTime":1306,"updateTime":1306,"relativeEntities":1323,"slug":1308,"properties":1324,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1325},{"EN":1311},{"openalex":1327,"title":1329},{"VOID":1328},"A5079745625",{"EN":1330},"Zsófia Szentpétery",{"id":1332,"sortIndex":111,"researcher":26,"roles":1333,"affiliations":1334,"properties":1340},"cf441307-de4a-4edc-97e3-38eb778c42b9",[],[1335],{"id":26,"sortIndex":36,"affiliation":1336,"properties":26},{"id":1305,"createTime":1306,"updateTime":1306,"relativeEntities":1337,"slug":1308,"properties":1338,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1339},{"EN":1311},{"openalex":1341,"orcid":1343,"title":1345},{"VOID":1342},"A5050743363",{"VOID":1344},"https:\u002F\u002Forcid.org\u002F0000-0002-9077-3335",{"EN":1346},"Tamás Balla",{"id":1348,"sortIndex":115,"researcher":26,"roles":1349,"affiliations":1350,"properties":1361},"553094a7-1f24-4f8e-8f6e-5bd6f0ce6910",[],[1351],{"id":26,"sortIndex":36,"affiliation":1352,"properties":26},{"id":1353,"createTime":1354,"updateTime":1355,"relativeEntities":1356,"slug":1357,"properties":1358,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"b696109e-c82a-4a39-971f-5dbb706356c0","2023-12-29T11:20:02.116+00:00","2025-02-09T14:22:04.259+00:00",[],"Department-of-Physiology-Semmelweis-University-School-of-Medicine-Budapest-Hungary",{"title":1359},{"VI":1360},"Department of Physiology, Semmelweis University School of Medicine, Budapest, Hungary",{"openalex":1362,"orcid":1364,"title":1366},{"VOID":1363},"A5042675661",{"VOID":1365},"https:\u002F\u002Forcid.org\u002F0000-0002-6450-2793",{"EN":1367},"András Balla",{"url":26,"publisher":1369,"properties":26},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":1370,"slug":663,"properties":1371,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":1375,"manageAffiliations":1376,"indexDatabases":1377,"url":26,"thumbnailPath":26,"statistic":1384,"gsStatistic":26,"type":175,"analyzePriority":26},[],{"issn":1372,"title":1373,"url":1374},{"VOID":666},{"EN":668},{"VOID":670},[],[],[1378],{"id":675,"indexDatabase":1379,"url":688,"indexYears":689,"academicFieldIds":26,"indexDatabaseRanking":690},{"id":677,"createTime":678,"updateTime":679,"relativeEntities":1380,"label":1381,"description":1382,"key":685,"publicationTags":1383,"standard":26},[],{"EN":682,"VI":682},{"EN":682,"VI":684},[687],{"impactFactor":36,"impactFactorByYear":1385,"i10Index":697,"i10IndexLast5Year":36,"totalPublication":698,"totalPublicationByYear":1386,"totalCitation":700,"totalCitationByYear":1387,"totalCitationPerPublication":712,"totalCitationPerPublicationByYear":1388,"hindexLast5Year":397,"hindex":397},{"2012":522,"2013":637,"2014":693,"2015":641,"2016":478,"2017":645,"2018":694,"2019":695,"2020":696},{"2000":114,"2001":356,"2002":238,"2003":52,"2004":79,"2005":240,"2006":260,"2007":252,"2008":539,"2009":623,"2010":568,"2011":48,"2012":240,"2013":252,"2014":240,"2015":336,"2016":260,"2017":239,"2018":234},{"2006":702,"2007":703,"2008":704,"2009":705,"2010":706,"2011":117,"2012":707,"2013":708,"2014":709,"2015":710,"2016":711,"2017":159,"2018":281},{"2006":714,"2007":715,"2008":716,"2009":717,"2010":718,"2011":719,"2012":720,"2013":721,"2014":722,"2015":723,"2016":724,"2017":725,"2018":726},{"total":361,"publishYear":26,"statisticByYear":1390},{"2012":298,"2013":158,"2014":162,"2015":116,"2016":50,"2017":111,"2018":52,"2019":158,"2020":50,"2021":53,"2022":52,"2023":50,"2024":115},"2009-12-01",2009,"ERROR_IN_ANALYZE_CITATION","2024-04-11T20:50:19.425+00:00",[1396,1399,1403,1407,1411,1415,1419,1423,1427,1431,1435,1439,1442,1446,1449,1453,1457,1461,1465,1469,1473,1477,1481,1485,1489,1493,1497,1501,1505,1509,1513,1517,1521,1525,1529,1533,1537,1541],{"id":26,"text":1397,"url":26,"identifiers":1398},"Berridge MJ: Inositol trisphosphate and diacylglycerol as intracellular messengers. 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J Cell Sci. 2008, 121 (Pt 5): 551-559. 10.1242\u002Fjcs.023333.",{"doi":1414},"10.1242\u002Fjcs.023333",{"id":26,"text":1416,"url":26,"identifiers":1417},"Raucher D, Stauffer T, Chen W, Shen K, Guo S, York JD, Sheetz MP, Meyer T: Phosphatidylinositol 4,5-bisphosphate functions as a second messenger that regulates cytoskeleton-plasma membrane adhesion. Cell. 2000, 100: 221-228. 10.1016\u002FS0092-8674(00)81560-3.",{"doi":1418},"10.1016\u002FS0092-8674(00)81560-3",{"id":26,"text":1420,"url":26,"identifiers":1421},"Irvine RF: Nuclear inositide signalling -- expansion, structures and clarification. Biochim Biophys Acta. 2006, 1761 (5-6): 505-508.",{"doi":1422},"10.1016\u002Fj.bbalip.2006.02.008",{"id":26,"text":1424,"url":26,"identifiers":1425},"Stauffer TP, Ahn S, Meyer T: Receptor-induced transient reduction in plasma membrane PtdIns(4,5)P2 concentration monitored in living cells. 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Science. 2006, 313 (5785): 347-351. 10.1126\u002Fscience.1129551.",{"doi":1524},"10.1126\u002Fscience.1129551",{"id":26,"text":1526,"url":26,"identifiers":1527},"Shi X, Basran J, Seward HE, Childs W, Bagshaw CR, Boxer SG: Anomalous negative fluorescence anisotropy in yellow fluorescent protein (YFP 10C): quantitative analysis of FRET in YFP dimers. Biochemistry. 2007, 46 (50): 14403-14417. 10.1021\u002Fbi701575n.",{"doi":1528},"10.1021\u002Fbi701575n",{"id":26,"text":1530,"url":26,"identifiers":1531},"Nash MS, Willets JM, Billups B, John Challiss RA, Nahorski SR: Synaptic activity augments muscarinic acetylcholine receptor-stimulated inositol 1,4,5-trisphosphate production to facilitate Ca2+ release in hippocampal neurons. 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Brain Res. 2005, 1055 (1-2): 60-72. 10.1016\u002Fj.brainres.2005.06.091.",{"doi":1540},"10.1016\u002Fj.brainres.2005.06.091",{"id":26,"text":1542,"url":26,"identifiers":1543},"Horowitz LF, Hirdes W, Suh BC, Hilgemann DW, Mackie K, Hille B: Phospholipase C in living cells: activation, inhibition, Ca2+ requirement, and regulation of M current. J Gen Physiol. 2005, 126 (3): 243-262. 10.1085\u002Fjgp.200509309.",{"doi":1544},"10.1085\u002Fjgp.200509309",{"id":1546,"createTime":1547,"updateTime":1548,"relativeEntities":1549,"slug":1550,"properties":1551,"entityType":756,"verifyStatus":25,"verifyTime":1569,"verifyNote":757,"syncStatus":28,"languages":1570,"translateLanguages":1571,"viewCount":36,"primaryUrl":1572,"fullTextUrl":26,"authors":1573,"publicationType":861,"publisherRelationship":1624,"citationCount":367,"citationInfo":1645,"publishDate":1647,"publishYear":1648,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1649,"isForceReanalyzing":997},"d1638f4f-69ae-4b7f-8ad5-1f0ebff690b8","2024-04-14T21:15:12.405+00:00","2025-02-17T21:11:36.619+00:00",[],"Dynamics-of-adipogenic-promoter-DNA-methylation-during-clonal-culture-of-human-adipose-stem-cells-to-senescence",{"mag":1552,"keywords":1554,"pmc":1555,"openalex":1557,"abstract":1559,"title":1562,"pm":1565,"doi":1567},{"VOID":1553},"1987527399",{"VI":741},{"VOID":1556},"1892011",{"VOID":1558},"W1987527399",{"EN":1560,"VI":1561},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>Potential therapeutic use of mesenchymal stem cells (MSCs) is likely to require large-scale in vitro expansion of the cells before transplantation. MSCs from adipose tissue can be cultured extensively until senescence. However, little is known on the differentiation potential of adipose stem cells (ASCs) upon extended culture and on associated epigenetic alterations. We examined the adipogenic differentiation potential of clones of human ASCs in early passage culture and upon senescence, and determined whether senescence was associated with changes in adipogenic promoter DNA methylation.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Results\u003C\u002Fjats:title>\n            \u003Cjats:p>ASC clones cultured to senescence display reduced adipogenic differentiation capacity in vitro, on the basis of limited lipogenesis and reduced transcriptional upregulation of \u003Cjats:italic>FABP4\u003C\u002Fjats:italic> and \u003Cjats:italic>LPL\u003C\u002Fjats:italic>, two adipogenic genes, while \u003Cjats:italic>LEP\u003C\u002Fjats:italic> and \u003Cjats:italic>PPARG2\u003C\u002Fjats:italic> transcription remains unaffected. In undifferentiated senescent cells, \u003Cjats:italic>PPARG2\u003C\u002Fjats:italic> and \u003Cjats:italic>LPL\u003C\u002Fjats:italic> expression is unaltered, whereas \u003Cjats:italic>LEP\u003C\u002Fjats:italic> and \u003Cjats:italic>FABP4\u003C\u002Fjats:italic> transcript levels are increased but not in all clones. Bisulfite sequencing analysis of DNA methylation reveals overall relative stability of \u003Cjats:italic>LEP\u003C\u002Fjats:italic>, \u003Cjats:italic>PPARG2\u003C\u002Fjats:italic>, \u003Cjats:italic>FABP4\u003C\u002Fjats:italic> and \u003Cjats:italic>LPL\u003C\u002Fjats:italic> promoter CpG methylation during senescence and upon differentiation. Mosaicism in methylation profiles is maintained between and within ASC clones, and any CpG-specific methylation change detected does not necessarily relate to differentiation potential. One exception to this contention is CpG No. 21 in the \u003Cjats:italic>LEP\u003C\u002Fjats:italic> promoter, whose senescence-related methylation may impair upregulation of the gene upon adipogenic stimulation.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n            \u003Cjats:p>Senescent ASCs display reduced in vitro differentiation ability and transcriptional activation of adipogenic genes upon differentiation induction. These restrictions, however, cannot in general be attributed to specific changes in DNA methylation at adipogenic promoters. There also seems to be a correlation between CpGs that are hypomethylated and important transcription factor binding sites.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Thông tin cơ bản\u003C\u002Fjats:title>\n            \u003Cjats:p>Các tế bào gốc trung mô (MSCs) có khả năng ứng dụng điều trị tiềm năng có thể cần phải mở rộng quy mô nuôi cấy in vitro trước khi cấy ghép. Các MSCs từ mô mỡ có thể được nuôi cấy mở rộng cho đến khi lão hóa. Tuy nhiên, vẫn còn rất ít thông tin về khả năng phân hóa của các tế bào gốc mỡ (ASCs) trong quá trình nuôi cấy kéo dài và các biến đổi dịch mã liên quan. Chúng tôi đã kiểm tra khả năng phân hóa thành mỡ của các dòng ASCs người trong nuôi cấy ở giai đoạn đầu và khi đến tuổi già, đồng thời xác định liệu sự lão hóa có liên quan đến các thay đổi trong methyl hóa DNA vùng khởi động adipogenic hay không.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết quả\u003C\u002Fjats:title>\n            \u003Cjats:p>Các dòng ASC được nuôi cấy đến tuổi già thể hiện khả năng phân hóa thành mỡ giảm trong điều kiện in vitro, dựa trên sự tổng hợp lipid hạn chế và giảm điều hòa gia tăng phiên mã của \u003Cjats:italic>FABP4\u003C\u002Fjats:italic> và \u003Cjats:italic>LPL\u003C\u002Fjats:italic>, hai gen adipogenic, trong khi phiên mã của \u003Cjats:italic>LEP\u003C\u002Fjats:italic> và \u003Cjats:italic>PPARG2\u003C\u002Fjats:italic> không bị ảnh hưởng. Trong các tế bào lão hóa không biệt hóa, biểu hiện của \u003Cjats:italic>PPARG2\u003C\u002Fjats:italic> và \u003Cjats:italic>LPL\u003C\u002Fjats:italic> không thay đổi, trong khi mức độ bản sao của \u003Cjats:italic>LEP\u003C\u002Fjats:italic> và \u003Cjats:italic>FABP4\u003C\u002Fjats:italic> tăng lên nhưng không ở tất cả các dòng. Phân tích trình tự bisulfite của methyl hóa DNA cho thấy mức độ ổn định tương đối của methyl hóa CpG ở vùng khởi động của \u003Cjats:italic>LEP\u003C\u002Fjats:italic>, \u003Cjats:italic>PPARG2\u003C\u002Fjats:italic>, \u003Cjats:italic>FABP4\u003C\u002Fjats:italic> và \u003Cjats:italic>LPL\u003C\u002Fjats:italic> trong quá trình lão hóa và khi phân hóa. Sự phân mảng trong các hồ sơ methyl hóa được duy trì giữa và trong các dòng ASC, và bất kỳ thay đổi methyl hóa CpG cụ thể nào được phát hiện không nhất thiết phải liên quan đến khả năng phân hóa. Một ngoại lệ cho luận điểm này là CpG số 21 trong vùng khởi động \u003Cjats:italic>LEP\u003C\u002Fjats:italic>, sự methyl hóa liên quan đến lão hóa của nó có thể cản trở việc điều hòa gia tăng gen khi bị kích thích phân hóa thành mỡ.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết luận\u003C\u002Fjats:title>\n            \u003Cjats:p>Các ASC ở trạng thái lão hóa thể hiện khả năng phân hóa in vitro giảm và khả năng kích hoạt phiên mã của các gen adipogenic khi được kích thích phân hóa. Tuy nhiên, các hạn chế này không thể được quy cho các thay đổi cụ thể trong methyl hóa DNA ở các vùng khởi động adipogenic. Cũng dường như tồn tại một mối tương quan giữa các CpG bị hypo-methyl hóa và các vị trí liên kết của yếu tố phiên mã quan trọng.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>",{"EN":1563,"VI":1564},"Dynamics of adipogenic promoter DNA methylation during clonal culture of human adipose stem cells to senescence","Động lực của methyl hóa DNA ở vùng khởi động adipogenic trong quá trình nuôi cấy dòng tế bào gốc mỡ người đến tuổi già",{"VOID":1566},"17535427",{"VOID":1568},"10.1186\u002F1471-2121-8-18","2024-12-18T04:50:14.100+00:00",[102],[101],"https:\u002F\u002Fbmcmolcellbiol.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2121-8-18",[1574,1592,1608],{"id":1575,"sortIndex":115,"researcher":26,"roles":1576,"affiliations":1577,"properties":1587},"205556b2-94c5-419b-a777-7379ae214991",[],[1578],{"id":26,"sortIndex":36,"affiliation":1579,"properties":26},{"id":1580,"createTime":1581,"updateTime":1581,"relativeEntities":1582,"slug":1583,"properties":1584,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"9ed09793-5b8b-4387-87cd-92a953ae8960","2024-04-14T21:15:12.431+00:00",[],"Institute-of-Basic-Medical-Sciences-Faculty-of-Medicine-University-of-Oslo-Blindern-Norway",{"title":1585},{"EN":1586},"Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Blindern, Norway",{"openalex":1588,"title":1590},{"VOID":1589},"A5062215685",{"EN":1591},"Andrew C. Boquest",{"id":1593,"sortIndex":114,"researcher":26,"roles":1594,"affiliations":1595,"properties":1601},"4bb66529-a722-4646-96ce-f22e3e052dd1",[],[1596],{"id":26,"sortIndex":36,"affiliation":1597,"properties":26},{"id":1580,"createTime":1581,"updateTime":1581,"relativeEntities":1598,"slug":1583,"properties":1599,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1600},{"EN":1586},{"openalex":1602,"orcid":1604,"title":1606},{"VOID":1603},"A5072506531",{"VOID":1605},"https:\u002F\u002Forcid.org\u002F0000-0002-5059-6901",{"EN":1607},"Philippe Collas",{"id":1609,"sortIndex":36,"researcher":26,"roles":1610,"affiliations":1611,"properties":1617},"113da052-cb6f-45bc-bd61-6d02d7117c41",[],[1612],{"id":26,"sortIndex":36,"affiliation":1613,"properties":26},{"id":1580,"createTime":1581,"updateTime":1581,"relativeEntities":1614,"slug":1583,"properties":1615,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1616},{"EN":1586},{"openalex":1618,"orcid":1620,"title":1622},{"VOID":1619},"A5005479598",{"VOID":1621},"https:\u002F\u002Forcid.org\u002F0000-0003-0329-916X",{"EN":1623},"Agate Noer",{"url":26,"publisher":1625,"properties":26},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":1626,"slug":663,"properties":1627,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":1631,"manageAffiliations":1632,"indexDatabases":1633,"url":26,"thumbnailPath":26,"statistic":1640,"gsStatistic":26,"type":175,"analyzePriority":26},[],{"issn":1628,"title":1629,"url":1630},{"VOID":666},{"EN":668},{"VOID":670},[],[],[1634],{"id":675,"indexDatabase":1635,"url":688,"indexYears":689,"academicFieldIds":26,"indexDatabaseRanking":690},{"id":677,"createTime":678,"updateTime":679,"relativeEntities":1636,"label":1637,"description":1638,"key":685,"publicationTags":1639,"standard":26},[],{"EN":682,"VI":682},{"EN":682,"VI":684},[687],{"impactFactor":36,"impactFactorByYear":1641,"i10Index":697,"i10IndexLast5Year":36,"totalPublication":698,"totalPublicationByYear":1642,"totalCitation":700,"totalCitationByYear":1643,"totalCitationPerPublication":712,"totalCitationPerPublicationByYear":1644,"hindexLast5Year":397,"hindex":397},{"2012":522,"2013":637,"2014":693,"2015":641,"2016":478,"2017":645,"2018":694,"2019":695,"2020":696},{"2000":114,"2001":356,"2002":238,"2003":52,"2004":79,"2005":240,"2006":260,"2007":252,"2008":539,"2009":623,"2010":568,"2011":48,"2012":240,"2013":252,"2014":240,"2015":336,"2016":260,"2017":239,"2018":234},{"2006":702,"2007":703,"2008":704,"2009":705,"2010":706,"2011":117,"2012":707,"2013":708,"2014":709,"2015":710,"2016":711,"2017":159,"2018":281},{"2006":714,"2007":715,"2008":716,"2009":717,"2010":718,"2011":719,"2012":720,"2013":721,"2014":722,"2015":723,"2016":724,"2017":725,"2018":726},{"total":367,"publishYear":26,"statisticByYear":1646},{"2012":52,"2013":162,"2014":50,"2015":135,"2016":158,"2017":50,"2018":111,"2019":135,"2020":59,"2021":158,"2022":59,"2023":115},"2007-12-01",2007,[1650,1654,1658,1662,1666,1670,1674,1678,1682,1686,1690,1693,1697,1701,1704,1708,1712,1716,1720,1724,1728,1732,1736,1740,1744,1748,1752,1756,1760,1764,1768,1772,1776,1779,1783,1787,1791,1795,1799,1803,1807,1811,1815,1819,1823,1827,1831,1835,1839,1843,1847,1851,1855,1859,1863,1867,1870],{"id":26,"text":1651,"url":26,"identifiers":1652},"Zuk PA, Zhu M, Mizuno H, Huang J, Futrell JW, Katz AJ, Benhaim P, Lorenz HP, Hedrick MH: Multilineage cells from human adipose tissue: implications for cell-based therapies. 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Proc Natl Acad Sci U S A. 2001, 98: 10839-10844. 10.1073\u002Fpnas.191225998.",{"doi":1842},"10.1073\u002Fpnas.191225998",{"id":26,"text":1844,"url":26,"identifiers":1845},"Esteller M: Aberrant DNA methylation as a cancer-inducing mechanism. Annu Rev Pharmacol Toxicol. 2005, 45: 629-656. 10.1146\u002Fannurev.pharmtox.45.120403.095832.",{"doi":1846},"10.1146\u002Fannurev.pharmtox.45.120403.095832",{"id":26,"text":1848,"url":26,"identifiers":1849},"Ushijima T, Okochi-Takada E: Aberrant methylations in cancer cells: where do they come from?. Cancer Sci. 2005, 96: 206-211. 10.1111\u002Fj.1349-7006.2005.00035.x.",{"doi":1850},"10.1111\u002Fj.1349-7006.2005.00035.x",{"id":26,"text":1852,"url":26,"identifiers":1853},"Bahar R, Hartmann CH, Rodriguez KA, Denny AD, Busuttil RA, Dolle ME, Calder RB, Chisholm GB, Pollock BH, Klein CA, Vijg J: Increased cell-to-cell variation in gene expression in ageing mouse heart. Nature. 2006, 441: 1011-1014. 10.1038\u002Fnature04844.",{"doi":1854},"10.1038\u002Fnature04844",{"id":26,"text":1856,"url":26,"identifiers":1857},"Hasty P, Campisi J, Hoeijmakers J, van SH, Vijg J: Aging and genome maintenance: lessons from the mouse?. Science. 2003, 299: 1355-1359. 10.1126\u002Fscience.1079161.",{"doi":1858},"10.1126\u002Fscience.1079161",{"id":26,"text":1860,"url":26,"identifiers":1861},"Roura S, Farre J, Soler-Botija C, Llach A, Hove-Madsen L, Cairo JJ, Godia F, Cinca J, Bayes-Genis A: Effect of aging on the pluripotential capacity of human CD105+ mesenchymal stem cells. 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Ensembl Human. 2007, [http:\u002F\u002Fwww.ensembl.org\u002FHomo_sapiens]",{},{"id":26,"text":1871,"url":26,"identifiers":1872},"MethPrimer - Design Primers for Methylation PCRs. 2007, [http:\u002F\u002Fwww.urogene.org\u002Fmethprimer\u002Findex1.html]",{},{"id":1874,"createTime":1875,"updateTime":1876,"relativeEntities":1877,"slug":1878,"properties":1879,"entityType":756,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":1897,"translateLanguages":1898,"viewCount":36,"primaryUrl":1899,"fullTextUrl":26,"authors":1900,"publicationType":861,"publisherRelationship":1967,"citationCount":258,"citationInfo":1988,"publishDate":1391,"publishYear":1392,"citationAnalyzeStatus":1393,"lastCitationAnalyze":1990,"indexDatabases":26,"openAccess":26,"references":1991,"isForceReanalyzing":997},"eb19c01d-6e3c-4b89-b76d-fd3138fc38d4","2024-04-11T22:46:41.632+00:00","2025-02-17T21:12:35.980+00:00",[],"Complete-reversal-of-epithelial-to-mesenchymal-transition-requires-inhibition-of-both-ZEB-expression-and-the-Rho-pathway",{"mag":1880,"keywords":1882,"pmc":1883,"openalex":1885,"abstract":1887,"title":1890,"pm":1893,"doi":1895},{"VOID":1881},"2171059311",{"VI":741},{"VOID":1884},"2806300",{"VOID":1886},"W2171059311",{"EN":1888,"VI":1889},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>Epithelial to Mesenchymal Transition (EMT) induced by Transforming Growth Factor-β (TGF-β) is an important cellular event in organogenesis, cancer, and organ fibrosis. The process to reverse EMT is not well established. Our purpose is to define signaling pathways and transcription factors that maintain the TGF-β-induced mesenchymal state.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Results\u003C\u002Fjats:title>\n            \u003Cjats:p>Inhibitors of five kinases implicated in EMT, TGF-β Type I receptor kinase (TβRI), p38 mitogen-activated protein kinase (p38 MAPK), MAP kinase kinase\u002Fextracellular signal-regulated kinase activator kinase (MEK1), c-Jun NH-terminal kinase (JNK), and Rho kinase (ROCK), were evaluated for reversal of the mesenchymal state induced in renal tubular epithelial cells. Single agents did not fully reverse EMT as determined by cellular morphology and gene expression. However, exposure to the TβRI inhibitor SB431542, combined with the ROCK inhibitor Y27632, eliminated detectable actin stress fibers and mesenchymal gene expression while restoring epithelial E-cadherin and Kidney-specific cadherin (Ksp-cadherin) expression. A second combination, the TβRI inhibitor SB431542 together with the p38 MAPK inhibitor SB203580, was partially effective in reversing EMT. Furthermore, JNK inhibitor SP600125 inhibits the effectiveness of the TβRI inhibitor SB431542 to reverse EMT. To explore the molecular basis underlying EMT reversal, we also targeted the transcriptional repressors ZEB1 and ZEB2\u002FSIP1. Decreasing ZEB1 and ZEB2 expression in mouse mammary gland cells with shRNAs was sufficient to up-regulate expression of epithelial proteins such as E-cadherin and to re-establish epithelial features. However, complete restoration of cortical F-actin required incubation with the ROCK inhibitor Y27632 in combination with ZEB1\u002F2 knockdown.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n            \u003Cjats:p>We demonstrate that reversal of EMT requires re-establishing both epithelial transcription and structural components by sustained and independent signaling through TβRI and ROCK. These findings indicate that combination small molecule therapy targeting multiple kinases may be necessary to reverse disease conditions.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Nền tảng\u003C\u002Fjats:title>\n            \u003Cjats:p>Quá trình chuyển đổi biểu mô sang trung mô (EMT) liên quan đến yếu tố tăng trưởng biến đổi-β (TGF-β) là một sự kiện tế bào quan trọng trong quá trình hình thành cơ quan, ung thư và xơ hóa cơ quan. Quy trình đảo ngược EMT vẫn chưa được thiết lập rõ ràng. Mục đích của chúng tôi là xác định các con đường truyền tín hiệu và các yếu tố phiên mã duy trì trạng thái trung mô do TGF-β gây ra.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết quả\u003C\u002Fjats:title>\n            \u003Cjats:p>Các chất ức chế năm loại kinase có liên quan đến EMT, bao gồm kinase thụ thể TGF-β loại I (TβRI), kinase p38 MAPK, kinase kinase MAP\u002Fextracellular signal-regulated kinase activator kinase (MEK1), kinase c-Jun NH-terminal (JNK), và kinase Rho (ROCK), đã được đánh giá về khả năng đảo ngược trạng thái trung mô được gây ra trong các tế bào biểu mô ống thận. Các tác nhân đơn lẻ không hoàn toàn đảo ngược EMT như được xác định bởi hình thái tế bào và biểu hiện gen. Tuy nhiên, việc tiếp xúc với chất ức chế TβRI SB431542, kết hợp với chất ức chế ROCK Y27632, đã loại bỏ các sợi căng stress actin có thể phát hiện và biểu hiện gen trung mô trong khi phục hồi biểu hiện E-cadherin và cadherin đặc hiệu thận (Ksp-cadherin). Một sự kết hợp thứ hai, chất ức chế TβRI SB431542 cùng với chất ức chế p38 MAPK SB203580, cũng có tác dụng một phần trong việc đảo ngược EMT. Hơn nữa, chất ức chế JNK SP600125 ức chế hiệu quả của chất ức chế TβRI SB431542 trong việc đảo ngược EMT. Để khám phá cơ sở phân tử dưới đây đảo ngược EMT, chúng tôi cũng đã nhắm đến các yếu tố ức chế phiên mã ZEB1 và ZEB2\u002FSIP1. Giảm biểu hiện ZEB1 và ZEB2 trong các tế bào tuyến vú của chuột bằng shRNAs đã đủ để tăng cường biểu hiện của các protein biểu mô như E-cadherin và khôi phục các đặc điểm biểu mô. Tuy nhiên, việc phục hồi hoàn toàn cortical F-actin cần phải ủ với chất ức chế ROCK Y27632 kết hợp với sự gõ của ZEB1\u002F2.",{"EN":1891,"VI":1892},"Complete reversal of epithelial to mesenchymal transition requires inhibition of both ZEB expression and the Rho pathway","Sự đảo ngược hoàn toàn quá trình chuyển đổi biểu mô sang trung mô yêu cầu ức chế cả sự biểu hiện của ZEB và con đường Rho",{"VOID":1894},"20025777",{"VOID":1896},"10.1186\u002F1471-2121-10-94",[102],[101],"https:\u002F\u002Fbmcmolcellbiol.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2121-10-94",[1901,1919,1937,1951],{"id":1902,"sortIndex":115,"researcher":26,"roles":1903,"affiliations":1904,"properties":1914},"d8f96878-fc80-491b-8602-54a759d1a9e7",[],[1905],{"id":26,"sortIndex":36,"affiliation":1906,"properties":26},{"id":1907,"createTime":1908,"updateTime":1908,"relativeEntities":1909,"slug":1910,"properties":1911,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"d54da5f2-b0be-48b9-9da2-e404aa69819c","2024-04-11T22:46:41.655+00:00",[],"Department-of-Medicine-University-of-Wisconsin-School-of-Medicine-and-Public-Health-600-Highland-Avenue-Madison-Wisconsin-53792-USA",{"title":1912},{"EN":1913},"Department of Medicine, University of Wisconsin School of Medicine and Public Health, 600 Highland Avenue, Madison, Wisconsin, 53792, USA",{"openalex":1915,"title":1917},{"VOID":1916},"A5032884901",{"EN":1918},"Bryan N. Becker",{"id":1920,"sortIndex":59,"researcher":26,"roles":1921,"affiliations":1922,"properties":1932},"14d28b57-69a1-4686-ac7e-c5a763b0eef7",[],[1923],{"id":26,"sortIndex":36,"affiliation":1924,"properties":26},{"id":1925,"createTime":1926,"updateTime":1926,"relativeEntities":1927,"slug":1928,"properties":1929,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"55d66c5f-15f0-411f-b4cd-4142cebc595a","2024-04-11T22:46:41.682+00:00",[],"McArdle-Laboratory-for-Cancer-Research-University-of-Wisconsin-School-of-Medicine-and-Public-Health-1400-University-Ave-Madison-Wisconsin-53706-USA",{"title":1930},{"EN":1931},"McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, 1400 University Ave, Madison, Wisconsin, 53706, USA",{"openalex":1933,"title":1935},{"VOID":1934},"A5022719891",{"EN":1936},"Janet E. Mertz",{"id":1938,"sortIndex":36,"researcher":26,"roles":1939,"affiliations":1940,"properties":1946},"917e301d-6562-4279-9458-17c71f9fc574",[],[1941],{"id":26,"sortIndex":36,"affiliation":1942,"properties":26},{"id":1925,"createTime":1926,"updateTime":1926,"relativeEntities":1943,"slug":1928,"properties":1944,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1945},{"EN":1931},{"openalex":1947,"title":1949},{"VOID":1948},"A5027194352",{"EN":1950},"Shreyas Das",{"id":1952,"sortIndex":114,"researcher":26,"roles":1953,"affiliations":1954,"properties":1960},"81ff822f-c678-4935-b373-15818c2c2e0a",[],[1955],{"id":26,"sortIndex":36,"affiliation":1956,"properties":26},{"id":1925,"createTime":1926,"updateTime":1926,"relativeEntities":1957,"slug":1928,"properties":1958,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1959},{"EN":1931},{"openalex":1961,"orcid":1963,"title":1965},{"VOID":1962},"A5069266537",{"VOID":1964},"https:\u002F\u002Forcid.org\u002F0000-0002-2770-9656",{"EN":1966},"F. M. Hoffmann",{"url":26,"publisher":1968,"properties":26},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":1969,"slug":663,"properties":1970,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":1974,"manageAffiliations":1975,"indexDatabases":1976,"url":26,"thumbnailPath":26,"statistic":1983,"gsStatistic":26,"type":175,"analyzePriority":26},[],{"issn":1971,"title":1972,"url":1973},{"VOID":666},{"EN":668},{"VOID":670},[],[],[1977],{"id":675,"indexDatabase":1978,"url":688,"indexYears":689,"academicFieldIds":26,"indexDatabaseRanking":690},{"id":677,"createTime":678,"updateTime":679,"relativeEntities":1979,"label":1980,"description":1981,"key":685,"publicationTags":1982,"standard":26},[],{"EN":682,"VI":682},{"EN":682,"VI":684},[687],{"impactFactor":36,"impactFactorByYear":1984,"i10Index":697,"i10IndexLast5Year":36,"totalPublication":698,"totalPublicationByYear":1985,"totalCitation":700,"totalCitationByYear":1986,"totalCitationPerPublication":712,"totalCitationPerPublicationByYear":1987,"hindexLast5Year":397,"hindex":397},{"2012":522,"2013":637,"2014":693,"2015":641,"2016":478,"2017":645,"2018":694,"2019":695,"2020":696},{"2000":114,"2001":356,"2002":238,"2003":52,"2004":79,"2005":240,"2006":260,"2007":252,"2008":539,"2009":623,"2010":568,"2011":48,"2012":240,"2013":252,"2014":240,"2015":336,"2016":260,"2017":239,"2018":234},{"2006":702,"2007":703,"2008":704,"2009":705,"2010":706,"2011":117,"2012":707,"2013":708,"2014":709,"2015":710,"2016":711,"2017":159,"2018":281},{"2006":714,"2007":715,"2008":716,"2009":717,"2010":718,"2011":719,"2012":720,"2013":721,"2014":722,"2015":723,"2016":724,"2017":725,"2018":726},{"total":258,"publishYear":26,"statisticByYear":1989},{"2012":53,"2013":50,"2014":52,"2015":50,"2016":50,"2017":103,"2018":111,"2019":162,"2020":162,"2021":59,"2022":114,"2023":111,"2024":115},"2024-04-12T03:42:57.941+00:00",[1992,1996,2000,2004,2008,2012,2016,2020,2024,2028,2032,2036,2040,2044,2048,2052,2056,2060,2064,2068,2072,2076,2080,2084,2088,2092,2096,2100,2104,2108,2112,2116,2120,2124,2128,2132,2136,2140,2144,2148,2152,2156,2160,2164,2168,2172,2176,2180,2184,2188,2192,2196,2200,2204,2208,2212,2216,2220,2224,2228,2231,2235,2239,2243,2247,2251,2255,2258,2262,2266,2270,2274,2278,2282,2286,2290,2294,2298,2302,2306,2310,2314,2318,2322,2326],{"id":26,"text":1993,"url":26,"identifiers":1994},"Savagner P: Leaving the neighborhood: molecular mechanisms involved during epithelial-mesenchymal transition. 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Clin Gastroenterol Hepatol. 2006, 4: 325-34. 10.1016\u002Fj.cgh.2005.11.013.",{"doi":2313},"10.1016\u002Fj.cgh.2005.11.013",{"id":26,"text":2315,"url":26,"identifiers":2316},"Tanihara H, Inatani M, Honjo M, Tokushige H, Azuma J, Araie M: Intraocular pressure-lowering effects and safety of topical administration of a selective ROCK inhibitor, SNJ-1656, in healthy volunteers. Arch Ophthalmol. 2008, 126: 309-15. 10.1001\u002Farchophthalmol.2007.76.",{"doi":2317},"10.1001\u002Farchophthalmol.2007.76",{"id":26,"text":2319,"url":26,"identifiers":2320},"Lee DY, Sugden B: The latent membrane protein 1 oncogene modifies B-cell physiology by regulating autophagy. Oncogene. 2008, 27: 2833-42. 10.1038\u002Fsj.onc.1210946.",{"doi":2321},"10.1038\u002Fsj.onc.1210946",{"id":26,"text":2323,"url":26,"identifiers":2324},"Ellison-Zelski SJ, Solodin NM, Alarig ET: Repression of ESR1 through actions of estrogen receptor alpha and Sin3A at the proximal promoter. Mol Cell Biol. 2009, 29: 4949-58. 10.1128\u002FMCB.00383-09.",{"doi":2325},"10.1128\u002FMCB.00383-09",{"id":26,"text":2327,"url":26,"identifiers":2328},"Livak KJ, Schmittgen TD: Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2001, 25: 402-8. 10.1006\u002Fmeth.2001.1262.",{"doi":2329},"10.1006\u002Fmeth.2001.1262",{"id":2331,"createTime":2332,"updateTime":2333,"relativeEntities":2334,"slug":2335,"properties":2336,"entityType":756,"verifyStatus":25,"verifyTime":2354,"verifyNote":757,"syncStatus":28,"languages":2355,"translateLanguages":2356,"viewCount":36,"primaryUrl":2357,"fullTextUrl":26,"authors":2358,"publicationType":861,"publisherRelationship":2517,"citationCount":2542,"citationInfo":2543,"publishDate":2545,"publishYear":2546,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2547,"isForceReanalyzing":997},"3a237ef3-7e7f-4e0f-8d99-1a4a342cd6c4","2024-04-19T20:54:14.620+00:00","2025-02-17T21:13:32.433+00:00",[],"Significantly-improved-precision-of-cell-migration-analysis-in-time-lapse-video-microscopy-through-use-of-a-fully-automated-tracking-system",{"mag":2337,"keywords":2339,"pmc":2340,"openalex":2342,"abstract":2344,"title":2347,"pm":2350,"doi":2352},{"VOID":2338},"1970464197",{"VI":741},{"VOID":2341},"2858025",{"VOID":2343},"W1970464197",{"EN":2345,"VI":2346},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>Cell motility is a critical parameter in many physiological as well as pathophysiological processes. In time-lapse video microscopy, manual cell tracking remains the most common method of analyzing migratory behavior of cell populations. In addition to being labor-intensive, this method is susceptible to user-dependent errors regarding the selection of \"representative\" subsets of cells and manual determination of precise cell positions.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Results\u003C\u002Fjats:title>\n            \u003Cjats:p>We have quantitatively analyzed these error sources, demonstrating that manual cell tracking of pancreatic cancer cells lead to mis-calculation of migration rates of up to 410%. In order to provide for objective measurements of cell migration rates, we have employed multi-target tracking technologies commonly used in radar applications to develop fully automated cell identification and tracking system suitable for high throughput screening of video sequences of unstained living cells.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n            \u003Cjats:p>We demonstrate that our automatic multi target tracking system identifies cell objects, follows individual cells and computes migration rates with high precision, clearly outperforming manual procedures.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Giới thiệu\u003C\u002Fjats:title>\n            \u003Cjats:p>Sự di động của tế bào là một tham số quan trọng trong nhiều quá trình sinh lý cũng như bệnh lý. Trong vi phim thời gian thực, việc theo dõi tế bào bằng tay vẫn là phương pháp phổ biến nhất để phân tích hành vi di cư của các quần thể tế bào. Ngoài việc mất nhiều công sức, phương pháp này còn dễ bị ảnh hưởng bởi các lỗi phụ thuộc vào người sử dụng liên quan đến việc chọn lựa các tập con \"đại diện\" của các tế bào và xác định vị trí tế bào một cách thủ công.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết quả\u003C\u002Fjats:title>\n            \u003Cjats:p>Chúng tôi đã phân tích định lượng các nguồn lỗi này, chứng minh rằng việc theo dõi tế bào bằng tay đối với tế bào ung thư tụy dẫn đến tính toán sai tỷ lệ di cư lên đến 410%. Để cung cấp các phép đo khách quan về tỷ lệ di cư của tế bào, chúng tôi đã sử dụng công nghệ theo dõi đa mục tiêu thường được sử dụng trong các ứng dụng radar để phát triển một hệ thống nhận diện và theo dõi tế bào hoàn toàn tự động phù hợp cho việc sàng lọc thông lượng cao các đoạn video của tế bào sống không nhuộm màu.",{"EN":2348,"VI":2349},"Significantly improved precision of cell migration analysis in time-lapse video microscopy through use of a fully automated tracking system","Cải thiện đáng kể độ chính xác của phân tích sự di chuyển của tế bào trong vi phim thời gian thực thông qua việc sử dụng hệ thống theo dõi hoàn toàn tự động",{"VOID":2351},"20377897",{"VOID":2353},"10.1186\u002F1471-2121-11-24","2024-12-22T20:45:52.182+00:00",[102],[101],"https:\u002F\u002Fbmcmolcellbiol.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2121-11-24",[2359,2380,2395,2416,2431,2446,2466,2483,2500],{"id":2360,"sortIndex":135,"researcher":26,"roles":2361,"affiliations":2362,"properties":2373},"bdf11e2e-376a-48e9-a2cb-6de6ee47945c",[],[2363],{"id":2364,"sortIndex":36,"affiliation":2365,"properties":26},"5521fb5a-fa46-419f-aa93-0a3061e73a6e",{"id":2366,"createTime":2367,"updateTime":2367,"relativeEntities":2368,"slug":2369,"properties":2370,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"3c01c644-023f-43fd-b889-a0283180f787","2024-04-19T20:54:14.672+00:00",[],"Clinic-of-Internal-Medicine-I-Medical-Centre-Ulm-University-Albert-Einstein-Allee-23-D-89081-Ulm-Germany",{"title":2371},{"EN":2372},"Clinic of Internal Medicine I, Medical Centre Ulm University, Albert-Einstein-Allee 23, D-89081, Ulm, Germany",{"openalex":2374,"orcid":2376,"title":2378},{"VOID":2375},"A5062163674",{"VOID":2377},"https:\u002F\u002Forcid.org\u002F0000-0003-3259-0810",{"EN":2379},"Thomas Seufferlein",{"id":2381,"sortIndex":111,"researcher":26,"roles":2382,"affiliations":2383,"properties":2390},"8d84b79f-5b49-4dc3-9d75-391a035c17a5",[],[2384],{"id":2385,"sortIndex":36,"affiliation":2386,"properties":26},"b9800c21-8ee6-491f-b030-db66d6deccc8",{"id":2366,"createTime":2367,"updateTime":2367,"relativeEntities":2387,"slug":2369,"properties":2388,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2389},{"EN":2372},{"openalex":2391,"title":2393},{"VOID":2392},"A5031368409",{"EN":2394},"Goetz von Wichert",{"id":2396,"sortIndex":114,"researcher":26,"roles":2397,"affiliations":2398,"properties":2409},"2c22677f-b444-4ffa-b359-5b320ff8b937",[],[2399],{"id":2400,"sortIndex":36,"affiliation":2401,"properties":26},"902d8b1a-d143-4b49-a3c9-09e9dec60532",{"id":2402,"createTime":2403,"updateTime":2403,"relativeEntities":2404,"slug":2405,"properties":2406,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"2a58dbf3-b8d3-4890-bec3-eb15395e8334","2024-04-19T20:54:14.654+00:00",[],"Research-group-of-Bioinformatics-and-Systems-Biology-Institute-of-Neural-Information-Processing-Ulm-University-Albert-Einstein-Allee-11-D-89081-Ulm-Germany",{"title":2407},{"EN":2408},"Research group of Bioinformatics and Systems Biology, Institute of Neural Information Processing, Ulm University, Albert-Einstein-Allee 11, D-89081, Ulm, Germany",{"openalex":2410,"orcid":2412,"title":2414},{"VOID":2411},"A5023494828",{"VOID":2413},"https:\u002F\u002Forcid.org\u002F0000-0002-9534-6295",{"EN":2415},"Johann M. 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Cell. 2007, 128 (1): 29-43. 10.1016\u002Fj.cell.2006.12.021.",{"doi":2551},"10.1016\u002Fj.cell.2006.12.021",{"id":26,"text":2553,"url":26,"identifiers":2554},"Heng JI, Nguyen L, Castro DS, Zimmer C, Wildner H, Armant O, Skowronska-Krawczyk D, Bedogni F, Matter JM, Hevner R: Neurogenin 2 controls cortical neuron migration through regulation of Rnd2. Nature. 2008, 455 (7209): 114-118. 10.1038\u002Fnature07198.",{"doi":2555},"10.1038\u002Fnature07198",{"id":26,"text":2557,"url":26,"identifiers":2558},"Martin P, Parkhurst SM: Parallels between tissue repair and embryo morphogenesis. Development. 2004, 131 (13): 3021-3034. 10.1242\u002Fdev.01253.",{"doi":2559},"10.1242\u002Fdev.01253",{"id":26,"text":2561,"url":26,"identifiers":2562},"Schneider IC, Haugh JM: Mechanisms of gradient sensing and chemotaxis: conserved pathways, diverse regulation. Cell Cycle. 2006, 5 (11): 1130-1134.",{"doi":2563},"10.4161\u002Fcc.5.11.2770",{"id":26,"text":2565,"url":26,"identifiers":2566},"Henrickson SE, Mempel TR, Mazo IB, Liu B, Artyomov MN, Zheng H, Peixoto A, Flynn MP, Senman B, Junt T: T cell sensing of antigen dose governs interactive behavior with dendritic cells and sets a threshold for T cell activation. Nat Immunol. 2008, 9 (3): 282-291. 10.1038\u002Fni1559.",{"doi":2567},"10.1038\u002Fni1559",{"id":26,"text":2569,"url":26,"identifiers":2570},"Jacobelli J, Bennett FC, Pandurangi P, Tooley AJ, Krummel MF: Myosin-IIA and ICAM-1 regulate the interchange between two distinct modes of T cell migration. J Immunol. 2009, 182 (4): 2041-2050. 10.4049\u002Fjimmunol.0803267.",{"doi":2571},"10.4049\u002Fjimmunol.0803267",{"id":26,"text":2573,"url":26,"identifiers":2574},"Tooley AJ, Gilden J, Jacobelli J, Beemiller P, Trimble WS, Kinoshita M, Krummel MF: Amoeboid T lymphocytes require the septin cytoskeleton for cortical integrity and persistent motility. Nat Cell Biol. 2009, 11 (1): 17-26. 10.1038\u002Fncb1808.",{"doi":2575},"10.1038\u002Fncb1808",{"id":26,"text":2577,"url":26,"identifiers":2578},"Rose DM, Alon R, Ginsberg MH: Integrin modulation and signaling in leukocyte adhesion and migration. Immunol Rev. 2007, 218: 126-134. 10.1111\u002Fj.1600-065X.2007.00536.x.",{"doi":2579},"10.1111\u002Fj.1600-065X.2007.00536.x",{"id":26,"text":2581,"url":26,"identifiers":2582},"Hanahan D, Weinberg RA: The hallmarks of cancer. 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Rev Polarogr. 2002, 48: 209-237.",{"doi":2946},"10.5189\u002Frevpolarography.48.209",{"id":26,"text":2948,"url":26,"identifiers":2949},"Raether H: Surface Plasmons on Smooth and Rough Surfaces and on Gratings. 1988, Berlin: Springer-Verlag",{"doi":2950},"10.1007\u002FBFb0048317",{"id":26,"text":2952,"url":26,"identifiers":2953},"Chen CS, Ostuni E, Whitesides GM, Ingber DE: Using Self-Assembled Monolayers to Pattern ECM Proteins and Cells on Substrates. Extracellular Matrix Protocols. Edited by: Streuli C, Grant M. 2000, New Jersey: Humana Press, 209-219.",{"doi":2954},"10.1385\u002F1-59259-063-2:209",{"id":26,"text":2956,"url":26,"identifiers":2957},"Keselowsky BG, Collard DM, Garcia AJ: Surface chemistry modulates fibronectin conformation and directs integrin binding and specificity to control cell adhesion. J Biomed Mater Res A. 2003, 66 (2): 247-259.",{"doi":2958},"10.1002\u002Fjbm.a.10537",{"id":26,"text":2960,"url":26,"identifiers":2961},"Renner L, Pompe T, Salchert K, Werner C: Dynamic alterations of fibronectin layers on copolymer substrates with graded physicochemical characteristics. Langmuir. 2004, 20 (7): 2928-2933.",{"doi":2962},"10.1021\u002Fla0362627",{"id":26,"text":2964,"url":26,"identifiers":2965},"Harpaz Y, Gerstein M, Chothia C: Volume Changes on Protein-Folding. Structure. 1994, 2 (7): 641-649.",{"doi":2966},"10.1016\u002FS0969-2126(00)00065-4",{"id":26,"text":2968,"url":26,"identifiers":2969},"El Kadi N, Taulier N, Le Huerou JY, Gindre M, Urbach W, Nwigwe I, Kahn PC, Waks M: Unfolding and refolding of bovine serum albumin at acid pH: Ultrasound and structural studies. Biophys J. 2006, 91 (9): 3397-3404.",{"doi":2970},"10.1529\u002Fbiophysj.106.088963",{"id":26,"text":2972,"url":26,"identifiers":2973},"Krishnan A, Cha P, Liu YH, Allara D, Vogler EA: Interfacial energetics of blood plasma and serum adsorption to a hydrophobic self-assembled monolayer surface. Biomaterials. 2006, 27 (17): 3187-3194.",{"doi":2974},"10.1016\u002Fj.biomaterials.2005.12.032",{"id":26,"text":2976,"url":26,"identifiers":2977},"Elliott JT, Tona A, Plant AL: Comparison of reagents for shape analysis of fixed cells by automated fluorescence microscopy. Cytometry A. 2003, 52 (2): 90-100.",{"doi":2978},"10.1002\u002Fcyto.a.10025",{"id":26,"text":2980,"url":26,"identifiers":2981},"Baneyx G, Baugh L, Vogel V: Coexisting conformations of fibronectin in cell culture imaged using fluorescence resonance energy transfer. Proc Natl Acad Sci USA. 2001, 98 (25): 14464-14468.",{"doi":2982},"10.1073\u002Fpnas.251422998",{"id":26,"text":2984,"url":26,"identifiers":2985},"Ohashi T, Kiehart DP, Erickson HP: Dynamics and elasticity of the fibronectin matrix in living cell culture visualized by fibronectin-green fluorescent protein. Proc Natl Acad Sci USA. 1999, 96 (5): 2153-2158.",{"doi":2986},"10.1073\u002Fpnas.96.5.2153",{"id":26,"text":2988,"url":26,"identifiers":2989},"Palecek SP, Huttenlocher A, Horwitz AF, Lauffenburger DA: Physical and biochemical regulation of integrin release during rear detachment of migrating cells. J Cell Sci. 1998, 111 (Pt 7): 929-940.",{"doi":2990},"10.1242\u002Fjcs.111.7.929",{"id":26,"text":2992,"url":26,"identifiers":2993},"Grinnell F: Focal adhesion sites and the removal of substratum-bound fibronectin. J Cell Biol. 1986, 103 (6 Pt 2): 2697-2706.",{"doi":2994},"10.1083\u002Fjcb.103.6.2697",{"id":26,"text":2996,"url":26,"identifiers":2997},"Dimilla PA, Stone JA, Quinn JA, Albelda SM, Lauffenburger DA: Maximal Migration of Human Smooth-Muscle Cells on Fibronectin and Type-Iv Collagen Occurs at an Intermediate Attachment Strength. J Cell Biol. 1993, 122 (3): 729-737.",{"doi":2998},"10.1083\u002Fjcb.122.3.729",{"id":26,"text":3000,"url":26,"identifiers":3001},"Siegel MR, Sisler HD: Inhibition of Protein Synthesis in Vitro by Cycloheximide. Nature. 1963, 200: 675-676.",{"doi":3002},"10.1038\u002F200675a0",{"id":26,"text":3004,"url":26,"identifiers":3005},"Giebel KF, Bechinger C, Herminghaus S, Riedel M, Leiderer P, Weiland U, Bastmeyer M: Imaging of cell\u002Fsubstrate contacts of living cells with surface plasmon resonance microscopy. Biophys J. 1999, 76 (1): 509-516.",{"doi":3006},"10.1016\u002FS0006-3495(99)77219-X",{"id":26,"text":3008,"url":26,"identifiers":3009},"Halter M, Tona A, Bhadriraju K, Plant AL, Elliott JT: Automated live cell imaging of green fluorescent protein degradation in individual fibroblasts. Cytometry A. 2007, 71 (10): 827-834.",{"doi":3010},"10.1002\u002Fcyto.a.20461",{"id":26,"text":3012,"url":26,"identifiers":3013},"Malacara D, Malacara Z: Microscopes. Handbook of Optical Design. 2004, New York: Marcel Dekker, Inc, 415-438. 2",{},{"id":26,"text":3015,"url":26,"identifiers":3016},"Ruemmele JA, Golden MS, Gao Y, Cornelius EM, Anderson ME, Postelnicu L, Georgiadis RM: Quantitative surface plasmon resonance imaging: a simple approach to automated angle scanning. 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Exp Cell Res. 1997, 235 (2): 305-313.",{"doi":3029},"10.1006\u002Fexcr.1997.3668",{"id":26,"text":3031,"url":26,"identifiers":3032},"Guemouri L, Ogier J, Ramsden JJ: Optical properties of protein monolayers during assembly. J Chem Phys. 1998, 109 (8): 3265-3268.",{"doi":3033},"10.1063\u002F1.476917",{"id":26,"text":3035,"url":26,"identifiers":3036},"Noda H: Partial Specific Volume of Collagen. J Biochem-Tokyo. 1972, 71 (4): 699-703.",{},{"id":26,"text":3038,"url":26,"identifiers":3039},"Model MA, Healy KE: Quantification of the surface density of a fluorescent label with the optical microscope. J Biomed Mater Res. 2000, 50 (1): 90-96.",{"doi":3040},"10.1002\u002F(SICI)1097-4636(200004)50:1\u003C90::AID-JBM13>3.0.CO;2-3",{"id":3042,"createTime":3043,"updateTime":3044,"relativeEntities":3045,"slug":3046,"properties":3047,"entityType":756,"verifyStatus":25,"verifyTime":3066,"verifyNote":757,"syncStatus":28,"languages":3067,"translateLanguages":3068,"viewCount":36,"primaryUrl":3069,"fullTextUrl":26,"authors":3070,"publicationType":861,"publisherRelationship":3149,"citationCount":357,"citationInfo":3170,"publishDate":1156,"publishYear":1157,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":3172,"isForceReanalyzing":997},"cf115ba2-b8b4-4727-a411-852ed84a80f8","2024-04-15T19:19:06.787+00:00","2025-02-17T21:14:30.963+00:00",[],"Nuclear-envelope-transmembrane-proteins-NETs-that-are-up-regulated-during-myogenesis",{"mag":3048,"keywords":3050,"pmc":3052,"openalex":3054,"abstract":3056,"title":3059,"pm":3062,"doi":3064},{"VOID":3049},"1940968102",{"VI":3051},"protein xuyên màng, màng hạt nhân, điểm nhấn tế bào, myoblast, sự phát triển cơ",{"VOID":3053},"1635557",{"VOID":3055},"W1940968102",{"EN":3057,"VI":3058},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>The nuclear lamina is a protein meshwork lining the inner nuclear membrane, which contains a polymer of nuclear lamins associated with transmembrane proteins of the inner nuclear membrane. The lamina is involved in nuclear structure, gene expression, and association of the cytoplasmic cytoskeleton with the nucleus. We previously identified a group of 67 novel putative nuclear envelope transmembrane proteins (NETs) in a large-scale proteomics analysis. Because mutations in lamina proteins have been linked to several human diseases affecting skeletal muscle, we examined NET expression during differentiation of C2C12 myoblasts. Our goal was to identify new nuclear envelope and lamina components whose expression is coordinated with muscle differentiation.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Results\u003C\u002Fjats:title>\n            \u003Cjats:p>Using transcriptional microarray analysis, we found that expression of 6 of the NETs significantly increases during myoblast differentiation. We confirmed these results using quantitative RT-PCR, and furthermore, found that all 6 NETs are expressed at high levels in adult mouse skeletal muscle relative to 9 other tissues examined. Using epitope-tagged cDNAs, we determined that the 5 NETs we could analyze (NETs 9, 25, 32, 37 and 39) all target to the nuclear envelope in C2C12 cells. Furthermore, the 3 NETs that we could analyze by immunoblotting were highly enriched in nuclear envelopes relative to microsomal membranes purified from mouse liver. Database searches showed that 4 of the 6 up-regulated NETs contain regions of homology to proteins previously linked to signaling.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n            \u003Cjats:p>This work identified 6 NETs that are predicted to have important functions in muscle development and\u002For maintenance from their expression patterns during myoblast differentiation and in mouse tissues. We confirmed that 5 of these NETs are authentic nuclear envelope proteins. Four members of this group have potential signaling functions at the NE, based on their sequence homologies.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Đặt vấn đề\u003C\u002Fjats:title>\n            \u003Cjats:p>Màng lamina hạt nhân là một mạng lưới protein bên trong màng nhân, bao gồm polymer của các lamin hạt nhân liên kết với các protein xuyên màng của màng hạt nhân trong. Lamina có vai trò trong cấu trúc hạt nhân, biểu hiện gen và sự liên kết của bộ xương tế bào chất với hạt nhân. Chúng tôi đã xác định được một nhóm 67 protein xuyên màng của màng hạt nhân (NETs) tiềm năng mới trong một phân tích proteomics quy mô lớn. Do các đột biến trong các protein lamina đã được liên kết với một vài bệnh lý ở người ảnh hưởng đến cơ xương, chúng tôi đã xem xét biểu hiện của NET trong quá trình biệt hóa của các tế bào cơ myoblast C2C12. Mục tiêu của chúng tôi là xác định các thành phần mới của màng hạt nhân và lamina có biểu hiện đồng bộ với sự biệt hóa của cơ.\n          \u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết quả\u003C\u002Fjats:title>\n            \u003Cjats:p>Bằng cách sử dụng phân tích microarray phiên mã, chúng tôi phát hiện rằng biểu hiện của 6 trong số các NET tăng lên đáng kể trong quá trình biệt hóa myoblast. Chúng tôi đã xác nhận những kết quả này bằng cách sử dụng RT-PCR định lượng, và hơn nữa, phát hiện rằng tất cả 6 NET đều được biểu hiện với mức độ cao ở cơ xương chuột trưởng thành so với 9 mô khác được kiểm tra. Sử dụng cDNA gắn thẻ epitop, chúng tôi đã xác định rằng 5 NET mà chúng tôi có thể phân tích (NETs 9, 25, 32, 37 và 39) đều nhắm đến màng hạt nhân trong các tế bào C2C12. Hơn nữa, 3 NET mà chúng tôi có thể phân tích bằng phương pháp blotting miễn dịch đã được làm giàu cao trong các màng hạt nhân so với màng vi hạt được tinh chế từ gan chuột. Các tìm kiếm cơ sở dữ liệu cho thấy 4 trong số 6 NET được tăng cường chứa các vùng đồng hình với các protein trước đây đã được liên kết với tín hiệu hóa.",{"EN":3060,"VI":3061},"Nuclear envelope transmembrane proteins (NETs) that are up-regulated during myogenesis","Các protein xuyên màng tế bào nhân (NETs) được tăng cường trong quá trình sinh cơ",{"VOID":3063},"17062158",{"VOID":3065},"10.1186\u002F1471-2121-7-38","2025-01-29T08:03:13.674+00:00",[102],[101],"https:\u002F\u002Fbmcmolcellbiol.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2121-7-38",[3071,3089,3105,3119,3135],{"id":3072,"sortIndex":36,"researcher":26,"roles":3073,"affiliations":3074,"properties":3084},"d28c589d-0811-4a10-9bae-699a765783b6",[],[3075],{"id":26,"sortIndex":36,"affiliation":3076,"properties":26},{"id":3077,"createTime":3078,"updateTime":3078,"relativeEntities":3079,"slug":3080,"properties":3081,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"244598f6-10fa-4fd3-8229-b8c03f8317a6","2024-04-15T19:19:06.836+00:00",[],"Department-of-Cell-Biology-The-Scripps-Research-Institute-10555-N-Torrey-Pines-Rd-La-Jolla-CA-92037-USA",{"title":3082},{"EN":3083},"Department of Cell Biology, The Scripps Research Institute, 10555 N. 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Expert Opin Ther Targets. 2006;10(1 Suppl):143–55.",{"doi":3739},"10.1517\u002F14728222.10.1.143",{"id":26,"text":3741,"url":26,"identifiers":3742},"Hattori N, Mochizuki S, Kishi K, Nakajima T, Takaishi H, D’Armiento J, Okada Y. MMP-13 plays a role in keratinocyte migration, angiogenesis, and contraction in mouse skin wound healing. Am J Pathol. 2009;175(2 Suppl):533–46.",{"doi":3743},"10.2353\u002Fajpath.2009.081080",{"id":26,"text":3745,"url":26,"identifiers":3746},"Liang CC, Park AY, Guan JL. In vitro scratch assay: a convenient and inexpensive method for analysis of cell migration in vitro. Nat Protoc. 2007;2(2 Suppl):329–33.",{"doi":3747},"10.1038\u002Fnprot.2007.30",{"id":26,"text":3749,"url":26,"identifiers":3750},"Hardarson T, Hanson C, Claesson M, Stenevi U. Time-lapse recordings of human corneal epithelial healing. 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Dermatol Surg. 2005;31:674–86.",{"doi":3763},"10.1097\u002F00042728-200506000-00011",{"id":26,"text":3765,"url":26,"identifiers":3766},"Stern R. Hyaluronan catabolism: a new metabolic pathway. Eur J Cell Biol. 2004;83(7 Suppl):317–25.",{"doi":3767},"10.1078\u002F0171-9335-00392",{"id":26,"text":3769,"url":26,"identifiers":3770},"Maneiro E, de Andres MC, Fernández-Sueiro JL, Galdo F, Blanco FJ. The biological action of hyaluronan on human osteoartritic articular chondrocytes: the importance of molecular weight. Clin Exp Rheumatol. 2004;22(3 Suppl):307–12.",{},{"id":26,"text":3772,"url":26,"identifiers":3773},"Walter MN, Wright KT, Fuller HR, MacNeil S, Johnson WE. Mesenchymal stem cell-conditioned medium accelerates skin wound healing: an in vitro study of fibroblast and keratinocyte scratch assays. Exp Cell Res. 2010;316(7):1271–81.",{"doi":3774},"10.1016\u002Fj.yexcr.2010.02.026",{"id":26,"text":3776,"url":26,"identifiers":3777},"Massagué J. TGF-β signal transduction. 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N Engl J Med. 1999;341(10 Suppl):738–46.",{"doi":3794},"10.1056\u002FNEJM199909023411006",{"id":3796,"createTime":3797,"updateTime":3798,"relativeEntities":3799,"slug":3800,"properties":3801,"entityType":756,"verifyStatus":25,"verifyTime":3798,"verifyNote":757,"syncStatus":28,"languages":3817,"translateLanguages":26,"viewCount":36,"primaryUrl":3818,"fullTextUrl":26,"authors":3819,"publicationType":861,"publisherRelationship":3972,"citationCount":3996,"citationInfo":3997,"publishDate":1156,"publishYear":1157,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":3999,"isForceReanalyzing":997},"18ceb7a4-7e80-4b73-914f-282e74f1871c","2024-04-17T10:25:34.319+00:00","2024-12-28T20:01:02.970+00:00",[],"Cellular-Notch-responsiveness-is-defined-by-phosphoinositide-3-kinase-dependent-signals",{"mag":3802,"keywords":3804,"pmc":3805,"openalex":3807,"abstract":3809,"title":3811,"pm":3813,"doi":3815},{"VOID":3803},"2119600157",{},{"VOID":3806},"1403772",{"VOID":3808},"W2119600157",{"EN":3810},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\u003Cjats:title>Background\u003C\u002Fjats:title>\u003Cjats:p>Notch plays a wide-ranging role in controlling cell fate, differentiation and development. The PI3K-Akt pathway is a similarly conserved signalling pathway which regulates processes such as differentiation, proliferation and survival. Mice with disrupted Notch and PI3K signalling show phenotypic similarities during haematopoietic cell development, suggesting functional interaction between these pathways.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>We show that cellular responsiveness to Notch signals depends on the activity of the PI3K-Akt pathway in cells as diverse as CHO cells, primary T-cells and hippocampal neurons. Induction of the endogenous PI3K-Akt pathway in CHO cells (by the insulin pathway), in T-cells (via TCR activation) or in neurons (via TrKB activation) potentiates Notch-dependent responses. We propose that the PI3K-Akt pathway exerts its influence on Notch primarily via inhibition of GSK3-beta, a kinase known to phosphorylate and regulate Notch signals.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\u003Cjats:p>The PI3K-Akt pathway acts as a \"gain control\" for Notch signal responses. Since physiological levels of intracellular Notch are often low, coincidence with PI3K-activation may be crucial for induction of Notch-dependent responses.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":3812},"Cellular Notch responsiveness is defined by phosphoinositide 3-kinase-dependent signals",{"VOID":3814},"16507111",{"VOID":3816},"10.1186\u002F1471-2121-7-10",[102],"https:\u002F\u002Fbmcmolcellbiol.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2121-7-10",[3820,3840,3857,3876,3891,3906,3921,3942,3957],{"id":3821,"sortIndex":111,"researcher":26,"roles":3822,"affiliations":3823,"properties":3835},"dfae2840-56ad-48fa-8b14-a97df41d84e6",[],[3824],{"id":3825,"sortIndex":36,"affiliation":3826,"properties":26},"24cfb034-24af-413c-a89e-a6d80542785c",{"id":3827,"createTime":3828,"updateTime":3829,"relativeEntities":3830,"slug":3831,"properties":3832,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"d29bd033-5f56-4c55-829e-ca3786b2c93f","2024-04-17T10:25:34.454+00:00","2025-02-06T12:54:14.941+00:00",[],"Centre-for-Neuroscience-Research-University-of-Edinburgh-Summerhall-Edinburgh-EH9-1QH-UK",{"title":3833},{"EN":3834},"Centre for Neuroscience Research, University of Edinburgh, Summerhall, Edinburgh, EH9 1QH, UK",{"openalex":3836,"title":3838},{"VOID":3837},"A5063200585",{"EN":3839},"Sofia Papadia",{"id":3841,"sortIndex":50,"researcher":26,"roles":3842,"affiliations":3843,"properties":3850},"d9cb5360-e956-4faf-8e7c-03106567226a",[],[3844],{"id":3845,"sortIndex":36,"affiliation":3846,"properties":26},"2a01fc22-a94c-4b70-ba36-73c959bdd9e5",{"id":3827,"createTime":3828,"updateTime":3829,"relativeEntities":3847,"slug":3831,"properties":3848,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":3849},{"EN":3834},{"openalex":3851,"orcid":3853,"title":3855},{"VOID":3852},"A5006025723",{"VOID":3854},"https:\u002F\u002Forcid.org\u002F0000-0002-7629-5314",{"EN":3856},"Giles E. 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