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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\":\". 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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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Sci., 31, 509, 10.1016\u002Fj.tibs.2006.07.005",{"doi":1128},"10.1016\u002Fj.tibs.2006.07.005",{"id":26,"text":1130,"url":26,"identifiers":1131},"Halliwell, 2000, Lancet, 355, 1179, 10.1016\u002FS0140-6736(00)02075-4",{"doi":1132},"10.1016\u002FS0140-6736(00)02075-4",{"id":26,"text":1134,"url":26,"identifiers":1135},"Halliwell, 2006, Plant Physiol., 141, 312, 10.1104\u002Fpp.106.077073",{"doi":1136},"10.1104\u002Fpp.106.077073",{"id":1138,"createTime":1139,"updateTime":1140,"relativeEntities":1141,"slug":1142,"properties":1143,"entityType":755,"verifyStatus":25,"verifyTime":1139,"verifyNote":756,"syncStatus":28,"languages":1159,"translateLanguages":1160,"viewCount":36,"primaryUrl":1161,"fullTextUrl":26,"authors":1162,"publicationType":799,"publisherRelationship":1201,"citationCount":1234,"citationInfo":1235,"publishDate":1237,"publishYear":1238,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1239,"isForceReanalyzing":851},"b404ad49-ec42-471c-9b86-a9d6ceba242e","2024-09-26T02:52:02.966+00:00","2025-02-11T19:07:45.331+00:00",[],"Stress-granules-sites-of-mRNA-triage-that-regulate-mRNA-stability-and-translatability",{"mag":1144,"keywords":1146,"openalex":1147,"abstract":1149,"title":1152,"pm":1155,"doi":1157},{"VOID":1145},"2052137498",{"VI":862},{"VOID":1148},"W2052137498",{"EN":1150,"VI":1151},"\u003Cjats:p>Mammalian stress granules (SGs) are cytoplasmic domains into which mRNAs are sorted dynamically in response to phosphorylation of eukaryotic initiation factor (eIF) 2α, a key regulatory step in translational initiation. The activation of one or more of the eIF2α kinases leads to SG assembly by decreasing the levels of eIF2-GTP-tRNAMet, the ternary complex that is normally required for loading the initiator methionine onto the 48 S preinitiation complex to begin translation. This stress-induced scarcity of eIF2-GTP-tRNAMet allows the RNA-binding proteins TIA-1 (T-cell internal antigen-1) and TIAR (TIA-1-related protein) to bind the 48 S complex in lieu of the ternary complex, thereby promoting polysome disassembly and the concurrent routing of the mRNA into a SG. The actual formation of SGs occurs upon auto-aggregation of the prion-like C-termini of TIA-1 proteins; this aggregation is reversed in vivo by overexpression of the heat-shock protein (HSP) chaperone HSP70. Remarkably, HSP70 mRNA is excluded from SGs and is preferentially translated during stress, indicating that the RNA composition of the SG is selective. Moreover, the effects of HSP70 on TIA aggregation suggest a feedback loop whereby HSP70 synthesis is auto-regulated. Proteins that promote mRNA stability [e.g. HuR (Hu protein R)] and destabilize mRNA [i.e. tristetraprolin (TTP)] are also recruited to SGs, suggesting that SGs effect a process of mRNA triage, by promoting polysome disassembly and routing mRNAs to cytoplasmic domains enriched for HuR and TTP. This model reveals connections between the eIF2α kinase system, mRNA stability and cellular chaperone levels.\u003C\u002Fjats:p>","\u003Cjats:p>Các tiểu thể căng thẳng (SGs) ở động vật có vú là những miền trong tế bào chất, nơi mà mRNA được phân loại một cách linh hoạt theo phản ứng với việc phosphoryl hóa yếu tố khởi đầu eukaryotic (eIF) 2α, một bước điều chỉnh quan trọng trong quá trình khởi đầu dịch mã. Việc kích hoạt một hoặc nhiều kinase eIF2α dẫn đến sự hình thành tiểu thể căng thẳng bằng cách giảm mức độ eIF2-GTP-tRNAMet, phức hợp ba thành phần thường cần thiết để tải methionine khởi đầu vào phức hợp tiền khởi đầu 48 S nhằm bắt đầu quá trình dịch mã. Tình trạng khan hiếm eIF2-GTP-tRNAMet do căng thẳng cho phép các protein liên kết RNA TIA-1 (antigen nội tại tế bào T-1) và TIAR (protein liên quan TIA-1) gắn kết với phức hợp 48 S thay cho phức hợp ba thành phần, do đó thúc đẩy sự phân tách polysome và đồng thời định hướng mRNA vào một tiểu thể căng thẳng. Sự hình thành thực sự của các tiểu thể căng thẳng xảy ra khi các đuôi C giống prion của protein TIA-1 tự động tập hợp lại; sự tập hợp này được đảo ngược in vivo bởi sự biểu hiện quá mức của protein chaperone sốc nhiệt (HSP) HSP70. Đáng chú ý, mRNA HSP70 bị loại trừ khỏi các tiểu thể căng thẳng và được dịch mã ưu tiên trong điều kiện căng thẳng, cho thấy rằng thành phần RNA của tiểu thể căng thẳng là có chọn lọc. Hơn nữa, các tác động của HSP70 lên sự tập hợp TIA gợi ý một chu trình phản hồi, trong đó tổng hợp HSP70 được tự điều chỉnh. Các protein thúc đẩy tính ổn định của mRNA [ví dụ: HuR (protein Hu R)] và không ổn định hóa mRNA [tức là tristetraprolin (TTP)] cũng được tuyển chọn vào các tiểu thể căng thẳng, cho thấy rằng các tiểu thể căng thẳng thực hiện một quá trình phân loại mRNA, bằng cách thúc đẩy sự phân tách polysome và định hướng mRNA tới các miền tế bào chất giàu HuR và TTP. Mô hình này tiết lộ những mối liên hệ giữa hệ thống kinase eIF2α, tính ổn định của mRNA và mức độ chaperone trong tế bào.\u003C\u002Fjats:p>",{"EN":1153,"VI":1154},"Stress granules: sites of mRNA triage that regulate mRNA stability and translatability","Các tiểu thể căng thẳng: địa điểm phân loại mRNA có vai trò điều tiết tính ổn định và khả năng dịch mã của 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Immunology and Allergy, Brigham and Women's Hospital, Smith 652, I Jimmy Fund Way, Boston, MA 02115, U.S.A.",{"openalex":1178,"orcid":1180,"title":1182},{"VOID":1179},"A5079494537",{"VOID":1181},"https:\u002F\u002Forcid.org\u002F0000-0001-5349-281X",{"EN":1183},"Paul Anderson",{"id":1185,"sortIndex":36,"researcher":26,"roles":1186,"affiliations":1187,"properties":1194},"ab766462-dd18-4290-bbd9-0d6a07b624f7",[],[1188],{"id":1189,"sortIndex":36,"affiliation":1190,"properties":26},"88e4d228-3fb7-42d7-8ab8-cc7fa0430da4",{"id":1170,"createTime":1171,"updateTime":1171,"relativeEntities":1191,"slug":1173,"properties":1192,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1193},{"EN":1176},{"openalex":1195,"orcid":1197,"title":1199},{"VOID":1196},"A5005784745",{"VOID":1198},"https:\u002F\u002Forcid.org\u002F0000-0002-8363-9816",{"EN":1200},"Nancy 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implications of nitric oxide, superoxide and peroxynitrite 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University of Alabama at Birmingham, Birmingham, Alabama, 35233 U.S.A.",{"openalex":1277,"title":1279},{"VOID":1278},"A5112792257",{"EN":1280},"John P. Crow",{"id":1282,"sortIndex":36,"researcher":26,"roles":1283,"affiliations":1284,"properties":1291},"6ad7f1d0-84ea-4822-ac40-ba37023c50fd",[],[1285],{"id":1286,"sortIndex":36,"affiliation":1287,"properties":26},"1f2b271c-9814-42e1-b36a-4cac768b1b07",{"id":1268,"createTime":1269,"updateTime":1270,"relativeEntities":1288,"slug":1272,"properties":1289,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1290},{"VI":1275},{"openalex":1292,"orcid":1294,"title":1296},{"VOID":1293},"A5010895814",{"VOID":1295},"https:\u002F\u002Forcid.org\u002F0000-0003-1855-4653",{"EN":1297},"Joseph S. Beckman",{"url":26,"publisher":1299,"properties":1324},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":1300,"slug":663,"properties":1301,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":1307,"manageAffiliations":1308,"indexDatabases":1309,"url":734,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":1302,"issn":1303,"introduce":1304,"eissn":1305,"title":1306},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[1310,1317],{"id":697,"indexDatabase":1311,"url":712,"indexYears":26,"academicFieldIds":1316,"indexDatabaseRanking":26},{"id":699,"createTime":700,"updateTime":701,"relativeEntities":1312,"label":1313,"description":1314,"key":708,"publicationTags":1315,"standard":26},[],{"EN":704,"VI":704},{"VI":706,"EN":707},[710,711],[714],{"id":716,"indexDatabase":1318,"url":729,"indexYears":730,"academicFieldIds":1323,"indexDatabaseRanking":733},{"id":718,"createTime":719,"updateTime":720,"relativeEntities":1319,"label":1320,"description":1321,"key":726,"publicationTags":1322,"standard":26},[],{"EN":723,"VI":723},{"EN":723,"VI":725},[728],[732],{"volume":1325,"pages":1327,"issue":1329},{"VOID":1326},"21",{"VOID":1328},"330-334",{"VOID":1330},"2",{"total":1234,"publishYear":26,"statisticByYear":1332},{"2012":51,"2013":234,"2014":53,"2015":298,"2016":116,"2017":111,"2018":52,"2019":336,"2020":116,"2021":135,"2022":135,"2023":135,"2024":111},"1993-05-01",1993,[],{"id":1337,"createTime":1338,"updateTime":1339,"relativeEntities":1340,"slug":1341,"properties":1342,"entityType":755,"verifyStatus":25,"verifyTime":1338,"verifyNote":756,"syncStatus":28,"languages":1358,"translateLanguages":1359,"viewCount":36,"primaryUrl":1360,"fullTextUrl":26,"authors":1361,"publicationType":799,"publisherRelationship":1384,"citationCount":1416,"citationInfo":1417,"publishDate":1419,"publishYear":1420,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1421,"isForceReanalyzing":851},"b97c4dee-7fbd-4a1f-8d31-b90917f9d32e","2024-10-13T23:34:22.083+00:00","2025-02-11T19:08:47.333+00:00",[],"Glyoxalase-I-structure-function-and-a-critical-role-in-the-enzymatic-defence-against-glycation",{"mag":1343,"keywords":1345,"openalex":1346,"abstract":1348,"title":1351,"pm":1354,"doi":1356},{"VOID":1344},"1997604729",{"VI":862},{"VOID":1347},"W1997604729",{"EN":1349,"VI":1350},"\u003Cjats:p>Glyoxalase I is part of the glyoxalase system present in the cytosol of cells. The glyoxalase system catalyses the conversion of reactive, acyclic α-oxoaldehydes into the corresponding α-hydroxyacids. Glyoxalase I catalyses the isomerization of the hemithioacetal, formed spontaneously from α-oxoaldehyde and GSH, to S-2-hydroxyacylglutathione derivatives [RCOCH(OH)-SG→RCH(OH)CO-SG], and in so doing decreases the steady-state concentrations of physiological α-oxoaldehydes and associated glycation reactions. Physiological substrates of glyoxalase I are methylglyoxal, glyoxal and other acyclic α-oxoaldehydes. Human glyoxalase I is a dimeric Zn2+ metalloenzyme of molecular mass 42 kDa. Glyoxalase I from Escherichia coli is a Ni2+ metalloenzyme. The crystal structures of human and E. coli glyoxalase I have been determined to 1.7 and 1.5 Å resolution. The Zn2+ site comprises two structurally equivalent residues from each domain – Gln-33A, Glu-99A, His-126B, Glu-172B and two water molecules. The Ni2+ binding site comprises His-5A, Glu-56A, His-74B, Glu-122B and two water molecules. The catalytic reaction involves base-catalysed shielded-proton transfer from C-1 to C-2 of the hemithioacetal to form an ene-diol intermediate and rapid ketonization to the thioester product. R- and S-enantiomers of the hemithioacetal are bound in the active site, displacing the water molecules in the metal ion primary co-ordination shell. It has been proposed that Glu-172 is the catalytic base for the S-substrate enantiomer and Glu-99 the catalytic base for the R-substrate enantiomer; Glu-172 then reprotonates the ene-diol stereospecifically to form the R-2-hydroxyacylglutathione product. By analogy with the human enzyme, Glu-56 and Glu-122 may be the bases involved in the catalytic mechanism of E. coli glyoxalase I. The suppression of α-oxoaldehyde-mediated glycation by glyoxalase I is particularly important in diabetes and uraemia, where α-oxoaldehyde concentrations are increased. Decreased glyoxalase I activity in situ due to the aging process and oxidative stress results in increased glycation and tissue damage. Inhibition of glyoxalase I pharmacologically with specific inhibitors leads to the accumulation of α-oxoaldehydes to cytotoxic levels; cell-permeable glyoxalase I inhibitors are antitumour and antimalarial agents. Glyoxalase I has a critical role in the prevention of glycation reactions mediated by methylglyoxal, glyoxal and other α-oxoaldehydes in vivo.\u003C\u002Fjats:p>","\u003Cjats:p>Glyoxalase I là một phần của hệ thống glyoxalase có mặt trong tế bào chất của các tế bào. Hệ thống glyoxalase xúc tác cho quá trình chuyển đổi các α-oxoaldehyde phản ứng, acyclic thành các α-hydroxyacid tương ứng. Glyoxalase I xúc tác cho việc đồng phân hóa của hemithioacetal, được hình thành một cách tự phát từ α-oxoaldehyde và GSH, thành các dẫn xuất S-2-hydroxyacylglutathione [RCOCH(OH)-SG→RCH(OH)CO-SG], từ đó làm giảm nồng độ ổn định của các α-oxoaldehyde sinh lý và các phản ứng glycation liên quan. Các chất nền sinh lý của glyoxalase I bao gồm methylglyoxal, glyoxal và các α-oxoaldehyde acyclic khác. Glyoxalase I ở người là một enzym metalloenzyme dimeric Zn2+ có khối lượng phân tử 42 kDa. Glyoxalase I từ Escherichia coli là một metalloenzyme Ni2+. Các cấu trúc tinh thể của glyoxalase I ở người và E. coli đã được xác định với độ phân giải lần lượt là 1.7 và 1.5 Å. Vị trí Zn2+ gồm hai dư lượng tương đương cấu trúc từ mỗi miền – Gln-33A, Glu-99A, His-126B, Glu-172B và hai phân tử nước. Vị trí liên kết Ni2+ bao gồm His-5A, Glu-56A, His-74B, Glu-122B và hai phân tử nước. Phản ứng xúc tác liên quan đến việc chuyển proton shielded từ C-1 đến C-2 của hemithioacetal sản sinh ra một trung gian ene-diol và nhanh chóng chuyển hóa thành sản phẩm thioester. Các enantiomer R- và S-của hemithioacetal được gắn vào vị trí hoạt động, thay thế các phân tử nước trong vỏ phối hợp chính của ion kim loại. Đã được đề xuất rằng Glu-172 là bazơ xúc tác cho enantiomer S-substrate và Glu-99 là bazơ xúc tác cho enantiomer R-substrate; Glu-172 sau đó sẽ tái proton hóa stereospecifically sản phẩm R-2-hydroxyacylglutathione. Theo tương tự với enzym ở người, Glu-56 và Glu-122 có thể là các bazơ liên quan đến cơ chế xúc tác của glyoxalase I ở E. coli. Việc ức chế glycation do α-oxoaldehyde gây ra bởi glyoxalase I là rất quan trọng trong bệnh tiểu đường và urê huyết, nơi mà nồng độ α-oxoaldehyde tăng lên. Giảm hoạt động glyoxalase I tại chỗ do quá trình lão hóa và stress oxy hóa dẫn đến tăng cường glycation và tổn thương mô. Việc ức chế glyoxalase I bằng thuốc với các chất ức chế cụ thể dẫn đến sự tích tụ của các α-oxoaldehyde lên mức độc tế bào; các chất ức chế glyoxalase I có khả năng xuyên tế bào là các tác nhân chống khối u và chống sốt rét. Glyoxalase I đóng vai trò quan trọng trong việc ngăn ngừa các phản ứng glycation do methylglyoxal, glyoxal và các α-oxoaldehyde khác trong cơ thể.\u003C\u002Fjats:p>",{"EN":1352,"VI":1353},"Glyoxalase I – structure, function and a critical role in the enzymatic defence against glycation","Glyoxalase I – cấu trúc, chức năng và vai trò quan trọng trong phòng ngừa enzym đối với quá trình glycation",{"VOID":1355},"14641060",{"VOID":1357},"10.1042\u002Fbst0311343",[102],[101],"https:\u002F\u002Fportlandpress.com\u002Fbiochemsoctrans\u002Farticle\u002F31\u002F6\u002F1343\u002F64515\u002FGlyoxalase-I-structure-function-and-a-critical",[1362],{"id":1363,"sortIndex":36,"researcher":26,"roles":1364,"affiliations":1365,"properties":1377},"4e31ed20-d6b8-48dd-9c21-2c8aab405377",[],[1366],{"id":1367,"sortIndex":36,"affiliation":1368,"properties":26},"b08ef941-ca87-45c0-84d4-c2d16fd6e6e1",{"id":1369,"createTime":1370,"updateTime":1371,"relativeEntities":1372,"slug":1373,"properties":1374,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"adfbb182-9e25-46af-a2a4-104471463f6a","2024-10-13T23:34:22.105+00:00","2025-02-02T03:49:02.265+00:00",[],"Department-of-Biological-Sciences-University-of-Essex-Central-Campus-Wivenhoe-Park-Colchester-Essex-CO4-3SQ-U-K-",{"title":1375},{"EN":1376},"Department of Biological Sciences, University of Essex, Central Campus, Wivenhoe Park, Colchester, Essex CO4 3SQ, U.K.",{"openalex":1378,"orcid":1380,"title":1382},{"VOID":1379},"A5056708838",{"VOID":1381},"https:\u002F\u002Forcid.org\u002F0000-0001-7659-443X",{"EN":1383},"Paul J. Thornalley",{"url":26,"publisher":1385,"properties":1410},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":1386,"slug":663,"properties":1387,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":1393,"manageAffiliations":1394,"indexDatabases":1395,"url":734,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":1388,"issn":1389,"introduce":1390,"eissn":1391,"title":1392},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[1396,1403],{"id":697,"indexDatabase":1397,"url":712,"indexYears":26,"academicFieldIds":1402,"indexDatabaseRanking":26},{"id":699,"createTime":700,"updateTime":701,"relativeEntities":1398,"label":1399,"description":1400,"key":708,"publicationTags":1401,"standard":26},[],{"EN":704,"VI":704},{"VI":706,"EN":707},[710,711],[714],{"id":716,"indexDatabase":1404,"url":729,"indexYears":730,"academicFieldIds":1409,"indexDatabaseRanking":733},{"id":718,"createTime":719,"updateTime":720,"relativeEntities":1405,"label":1406,"description":1407,"key":726,"publicationTags":1408,"standard":26},[],{"EN":723,"VI":723},{"EN":723,"VI":725},[728],[732],{"volume":1411,"pages":1413,"issue":1415},{"VOID":1412},"31",{"VOID":1414},"1343-1348",{"VOID":1233},600,{"total":1416,"publishYear":26,"statisticByYear":1418},{"2012":397,"2013":539,"2014":168,"2015":240,"2016":398,"2017":539,"2018":222,"2019":244,"2020":159,"2021":125,"2022":237,"2023":124,"2024":51},"2003-12-01",2003,[],{"id":1423,"createTime":1424,"updateTime":1425,"relativeEntities":1426,"slug":1427,"properties":1428,"entityType":755,"verifyStatus":25,"verifyTime":1424,"verifyNote":756,"syncStatus":28,"languages":1440,"translateLanguages":1441,"viewCount":36,"primaryUrl":1442,"fullTextUrl":26,"authors":1443,"publicationType":799,"publisherRelationship":1465,"citationCount":1497,"citationInfo":1498,"publishDate":1500,"publishYear":1501,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1502,"isForceReanalyzing":851},"2e4a2932-e363-411b-8be8-b8ec97f4270a","2024-10-03T18:51:32.616+00:00","2025-02-11T19:09:45.019+00:00",[],"Rho-GTPases-and-the-control-of-cell-behaviour",{"keywords":1429,"openalex":1430,"abstract":1432,"title":1435,"doi":1438},{"VI":862},{"VOID":1431},"W4248277281",{"EN":1433,"VI":1434},"\u003Cjats:p>Rho, Rac and Cdc42, three members of the Rho family of small GTPases, each control a signal transduction pathway linking membrane receptors to the assembly and disassembly of the actin cytoskeleton and of associated integrin adhesion complexes. Rho regulates stress fibre and focal adhesion assembly, Rac regulates the formation of lamellipodia protrusions and membrane ruffles, and Cdc42 triggers filopodial extensions at the cell periphery. These observations have led to the suggestion that wherever filamentous actin is used to drive a cellular process, Rho GTPases are likely to play an important regulatory role. Rho GTPases have also been reported to control other cellular activities, such as the JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase) cascades, an NADPH oxidase enzyme complex, the transcription factors NF-κB (nuclear factor κB) and SRF (serum-response factor), and progression through G1 of the cell cycle. Thus Rho, Rac and Cdc42 can regulate the actin cytoskeleton and gene transcription to promote co-ordinated changes in cell behaviour. We have been analysing the biochemical contributions of Rho GTPases in cell movement and have found that Rac controls cell protrusion, while Cdc42 controls cell polarity.\u003C\u002Fjats:p>","\u003Cjats:p>Rho, Rac và Cdc42, ba thành viên của gia đình GTPase nhỏ Rho, mỗi loại đều điều khiển một con đường truyền tín hiệu liên kết các thụ thể màng với sự lắp ráp và tháo dỡ của hệ thống tế bào chất actin và các phức hợp liên kết integrin liên quan. Rho điều chỉnh sự lắp ráp của các sợi căng và điểm bám tập trung, Rac điều chỉnh sự hình thành các chồi lamellipodia và các cuộn màng, và Cdc42 kích hoạt sự mở rộng filopodia ở ngoại vi của tế bào. Những quan sát này đã dẫn đến gợi ý rằng bất kể nơi nào mà actin sợi được sử dụng để thúc đẩy một quá trình tế bào, thì GTPase Rho có khả năng đóng vai trò điều tiết quan trọng. Các GTPase Rho cũng được báo cáo là kiểm soát các hoạt động tế bào khác, chẳng hạn như các chuỗi phản ứng JNK (kinase N-terminal c-Jun) và p38 MAPK (kinase protein hoạt hóa bởi tác nhân gây tăng sinh), một phức hợp enzyme NADPH oxidase, các yếu tố phiên mã NF-κB (yếu tố hạt nhân κB) và SRF (yếu tố phản ứng huyết thanh), và sự phát triển qua G1 của chu kỳ tế bào. Do đó, Rho, Rac và Cdc42 có thể điều chỉnh hệ thống tế bào chất actin và phiên mã gene để thúc đẩy những thay đổi phối hợp trong hành vi của tế bào. Chúng tôi đã phân tích các đóng góp sinh hóa của các GTPase Rho trong chuyển động tế bào và đã phát hiện rằng Rac điều khiển sự nhô ra của tế bào, trong khi Cdc42 điều khiển tính phân cực của tế bào.\u003C\u002Fjats:p>",{"EN":1436,"VI":1437},"Rho GTPases and the control of cell behaviour","Các GTPase Rho và sự điều khiển hành vi của tế bào",{"VOID":1439},"10.1042\u002Fbst0330891",[102],[101],"https:\u002F\u002Fportlandpress.com\u002Fbiochemsoctrans\u002Farticle\u002F33\u002F5\u002F891\u002F65120\u002FRho-GTPases-and-the-control-of-cell-behaviour",[1444],{"id":1445,"sortIndex":36,"researcher":26,"roles":1446,"affiliations":1447,"properties":1458},"87040a93-fb52-4f78-9213-a17af253b206",[],[1448],{"id":1449,"sortIndex":36,"affiliation":1450,"properties":26},"018abc2c-520c-4115-9101-23916b9b74e4",{"id":1451,"createTime":1452,"updateTime":1452,"relativeEntities":1453,"slug":1454,"properties":1455,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"b90aec30-a22d-455b-a73d-b335d64243fd","2024-10-03T18:51:32.635+00:00",[],"MRC-Laboratory-for-Molecular-Cell-Biology-and-Department-of-Biochemistry-and-Molecular-Biology-Cancer-Research-UK-Oncogene-and-Signal-Transduction-Group-University-College-London-Gower-Street-London-WC1E-6BT-U-K-",{"title":1456},{"EN":1457},"MRC Laboratory for Molecular Cell Biology and Department of Biochemistry and Molecular Biology, Cancer Research UK Oncogene and Signal Transduction Group, University College London, Gower Street, London WC1E 6BT, U.K.",{"openalex":1459,"orcid":1461,"title":1463},{"VOID":1460},"A5005908423",{"VOID":1462},"https:\u002F\u002Forcid.org\u002F0000-0002-7237-7945",{"EN":1464},"Alison K. Hall",{"url":26,"publisher":1466,"properties":1491},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":1467,"slug":663,"properties":1468,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":1474,"manageAffiliations":1475,"indexDatabases":1476,"url":734,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":1469,"issn":1470,"introduce":1471,"eissn":1472,"title":1473},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[1477,1484],{"id":697,"indexDatabase":1478,"url":712,"indexYears":26,"academicFieldIds":1483,"indexDatabaseRanking":26},{"id":699,"createTime":700,"updateTime":701,"relativeEntities":1479,"label":1480,"description":1481,"key":708,"publicationTags":1482,"standard":26},[],{"EN":704,"VI":704},{"VI":706,"EN":707},[710,711],[714],{"id":716,"indexDatabase":1485,"url":729,"indexYears":730,"academicFieldIds":1490,"indexDatabaseRanking":733},{"id":718,"createTime":719,"updateTime":720,"relativeEntities":1486,"label":1487,"description":1488,"key":726,"publicationTags":1489,"standard":26},[],{"EN":723,"VI":723},{"EN":723,"VI":725},[728],[732],{"volume":1492,"pages":1494,"issue":1496},{"VOID":1493},"33",{"VOID":1495},"891-895",{"VOID":832},539,{"total":1497,"publishYear":26,"statisticByYear":1499},{"2012":252,"2013":159,"2014":287,"2015":51,"2016":51,"2017":242,"2018":103,"2019":173,"2020":516,"2021":237,"2022":53,"2023":124,"2024":51},"2005-10-26",2005,[1503,1507,1511,1515,1519,1522,1526,1530,1534,1538,1542,1546,1550,1554,1558,1562,1566,1570,1574,1578,1582,1586,1590,1594,1598,1602,1606,1610,1614,1618,1622,1626],{"id":26,"text":1504,"url":26,"identifiers":1505},"Hall, 1998, Science, 279, 509, 10.1126\u002Fscience.279.5350.509",{"doi":1506},"10.1126\u002Fscience.279.5350.509",{"id":26,"text":1508,"url":26,"identifiers":1509},"Cerione, 1996, Curr. Opin. Cell Biol., 8, 216, 10.1016\u002FS0955-0674(96)80068-8",{"doi":1510},"10.1016\u002FS0955-0674(96)80068-8",{"id":26,"text":1512,"url":26,"identifiers":1513},"Schmidt, 2002, Genes Dev., 16, 1587, 10.1101\u002Fgad.1003302",{"doi":1514},"10.1101\u002Fgad.1003302",{"id":26,"text":1516,"url":26,"identifiers":1517},"Cote, 2002, J. Cell Sci., 115, 4901, 10.1242\u002Fjcs.00219",{"doi":1518},"10.1242\u002Fjcs.00219",{"id":26,"text":1520,"url":26,"identifiers":1521},"Bernards, 2003, Biochim. Biophys. Acta, 1603, 47",{},{"id":26,"text":1523,"url":26,"identifiers":1524},"Ridley, 1992, Cell, 70, 389, 10.1016\u002F0092-8674(92)90163-7",{"doi":1525},"10.1016\u002F0092-8674(92)90163-7",{"id":26,"text":1527,"url":26,"identifiers":1528},"Ridley, 1992, Cell, 70, 401, 10.1016\u002F0092-8674(92)90164-8",{"doi":1529},"10.1016\u002F0092-8674(92)90164-8",{"id":26,"text":1531,"url":26,"identifiers":1532},"Nobes, 1995, Cell, 81, 53, 10.1016\u002F0092-8674(95)90370-4",{"doi":1533},"10.1016\u002F0092-8674(95)90370-4",{"id":26,"text":1535,"url":26,"identifiers":1536},"Kozma, 1995, Mol. Cell. 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Biol., 10, 697, 10.1016\u002FS0960-9822(00)00535-2",{"doi":1621},"10.1016\u002FS0960-9822(00)00535-2",{"id":26,"text":1623,"url":26,"identifiers":1624},"Etienne-Manneville, 2001, Cell, 106, 489, 10.1016\u002FS0092-8674(01)00471-8",{"doi":1625},"10.1016\u002FS0092-8674(01)00471-8",{"id":26,"text":1627,"url":26,"identifiers":1628},"Etienne-Manneville, 2003, Nature (London), 421, 753, 10.1038\u002Fnature01423",{"doi":1629},"10.1038\u002Fnature01423",{"id":1631,"createTime":1632,"updateTime":1633,"relativeEntities":1634,"slug":1635,"properties":1636,"entityType":755,"verifyStatus":25,"verifyTime":1632,"verifyNote":756,"syncStatus":28,"languages":1652,"translateLanguages":1653,"viewCount":36,"primaryUrl":1654,"fullTextUrl":26,"authors":1655,"publicationType":799,"publisherRelationship":1712,"citationCount":1744,"citationInfo":1745,"publishDate":1747,"publishYear":1748,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1749,"isForceReanalyzing":851},"59a5c67e-8b73-4550-8a5f-30014a89c183","2024-09-04T10:32:59.915+00:00","2025-02-11T19:10:46.198+00:00",[],"Signalling-through-Class-I-PI3Ks-in-mammalian-cells",{"mag":1637,"keywords":1639,"openalex":1640,"abstract":1642,"title":1645,"pm":1648,"doi":1650},{"VOID":1638},"1988224683",{"VI":862},{"VOID":1641},"W1988224683",{"EN":1643,"VI":1644},"\u003Cjats:p>It is now accepted that activation of Class I PI3Ks (phosphoinositide 3-kinases) is one of the most important signal transduction pathways used by cell-surface receptors to control intracellular events. The receptors which access this pathway include those that recognize growth factors, hormones, antigens and inflammatory stimuli, and the cellular events known to be regulated include cell growth, survival, proliferation and movement. We have learnt a great deal about the family of Class I PI3K enzymes themselves and the structural adaptations which allow a variety of cell-surface receptors to regulate their activity. Class I PI3Ks synthesize the phospholipid PtdIns(3,4,5)P3 in the membranes in which they are activated, and it is now accepted that PtdIns(3,4,5)P3 and its dephosphorylation product PtdIns(3,4)P2 are messenger molecules which regulate the localization and function of multiple effectors by binding to their specific PH (pleckstrin homology) domains. The number of direct PtdIns(3,4,5)P3\u002FPtdIns(3,4)P2 effectors which exist, even within a single cell, creates an extremely complex signalling web downstream of PI3K activation. Some key players are beginning to emerge, however, linking PI3K activity to specific cellular responses. These include small GTPases for the Rho and Arf families which regulate the cytoskeletal and membrane rearrangements required for cell movement, and PKB (protein kinase B), which has important regulatory inputs into the regulation of cell-cycle progression and survival. The importance of the PI3K signalling pathway in regulating the balance of decisions in cell growth, proliferation and survival is clear from the prevalence of oncogenes (e.g. PI3Kα) and tumour suppressors [e.g. the PtdIns(3,4,5)P3 3-phosphatase, PTEN (phosphatase and tensin homologue deleted on chromosome 10)] found in this pathway. The recent availability of transgenic mouse models with engineered defects in Class I PI3K signalling pathways, and the development of PI3K isoform-selective inhibitors by both academic and pharmaceutical research has highlighted the importance of specific isoforms of PI3K in whole-animal physiology and pathology, e.g. PI3Kα in growth and metabolic regulation, PI3Kβ in thrombosis, and PI3Kδ and PI3Kγ in inflammation and asthma. Thus the Class I PI3K signalling pathway is emerging as an exciting new area for the development of novel therapeutics.\u003C\u002Fjats:p>","\u003Cjats:p>Hiện nay, việc kích hoạt Class I PI3Ks (phosphoinositide 3-kinases) được chấp nhận là một trong những con đường truyền tín hiệu quan trọng nhất mà các thụ thể bề mặt tế bào sử dụng để điều khiển các sự kiện bên trong tế bào. Các thụ thể có thể truy cập vào con đường này bao gồm những thụ thể nhận diện yếu tố tăng trưởng, hormone, kháng nguyên và kích thích viêm, và các sự kiện tế bào được biết đến để điều chỉnh bao gồm sự phát triển tế bào, sự sống sót, sự phát triển và di chuyển. Chúng ta đã học được rất nhiều về họ enzyme Class I PI3K và những thích nghi cấu trúc cho phép nhiều thụ thể bề mặt tế bào khác nhau điều chỉnh hoạt động của chúng. Class I PI3Ks tổng hợp phospholipid PtdIns(3,4,5)P3 trong các màng mà chúng được kích hoạt, và hiện nay đã được chấp nhận rằng PtdIns(3,4,5)P3 và sản phẩm dephosphorylation của nó là PtdIns(3,4)P2 là những phân tử truyền tin điều chỉnh vị trí và chức năng của nhiều yếu tố tác động thông qua việc gắn kết với các miền PH (pleckstrin homology) cụ thể của chúng. Số lượng các yếu tố tác động PtdIns(3,4,5)P3\u002FPtdIns(3,4)P2 trực tiếp tồn tại, thậm chí trong cùng một tế bào, tạo ra một mạng lưới tín hiệu hết sức phức tạp ở phía hạ lưu của việc kích hoạt PI3K. Tuy nhiên, một số nhân tố chính đang bắt đầu xuất hiện, liên kết hoạt động của PI3K với các phản ứng tế bào cụ thể. Những yếu tố này bao gồm các GTPase nhỏ cho các họ Rho và Arf điều chỉnh sự tái sắp xếp cytoskeletal và màng cần thiết cho sự di chuyển của tế bào, và PKB (protein kinase B), có vai trò điều chỉnh quan trọng trong quản lý quá trình tiến triển chu kỳ tế bào và sự sống sót. Tầm quan trọng của con đường tín hiệu PI3K trong việc điều chỉnh sự cân bằng giữa các quyết định trong sự phát triển tế bào, sinh sản và sự sống sót là rõ ràng từ sự phổ biến của các oncogene (ví dụ PI3Kα) và các tác nhân ức chế khối u [ví dụ như PtdIns(3,4,5)P3 3-phosphatase, PTEN (phosphatase and tensin homologue deleted on chromosome 10)] được tìm thấy trong con đường này. Việc gần đây có sẵn các mô hình chuột chuyển gen với các khiếm khuyết được thiết kế trong các con đường tín hiệu Class I PI3K, và sự phát triển của các chất ức chế chọn lọc isoform PI3K bởi cả nghiên cứu học thuật và dược phẩm đã làm nổi bật tầm quan trọng của các isoform cụ thể của PI3K trong sinh lý học và bệnh lý toàn thân, ví dụ như PI3Kα trong điều hòa tăng trưởng và chuyển hóa, PI3Kβ trong cục máu đông, và PI3Kδ và PI3Kγ trong viêm và hen suyễn. Do đó, con đường tín hiệu Class I PI3K đang nổi lên như một lĩnh vực mới thú vị cho sự phát triển của các liệu pháp điều trị mới.\u003C\u002Fjats:p>",{"EN":1646,"VI":1647},"Signalling through Class I PI3Ks in mammalian cells","Tín hiệu thông qua Class I PI3Ks trong tế bào động vật có vú",{"VOID":1649},"17052169",{"VOID":1651},"10.1042\u002Fbst0340647",[102],[101],"https:\u002F\u002Fportlandpress.com\u002Fbiochemsoctrans\u002Farticle\u002F34\u002F5\u002F647\u002F66084\u002FSignalling-through-Class-I-PI3Ks-in-mammalian",[1656,1678,1695],{"id":1657,"sortIndex":114,"researcher":26,"roles":1658,"affiliations":1659,"properties":1671},"b9f0eabf-cb9b-4aba-9ffd-95d0ef934fb3",[],[1660],{"id":1661,"sortIndex":36,"affiliation":1662,"properties":26},"643a6f2d-b39d-4d52-8cc5-f776c8e38601",{"id":1663,"createTime":1664,"updateTime":1665,"relativeEntities":1666,"slug":1667,"properties":1668,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"00e0f85e-a13f-49a2-89af-8de192aa02c3","2024-09-04T10:32:59.948+00:00","2025-06-11T14:21:52.945+00:00",[],"The-Babraham-Institute-Babraham-Research-Campus-Babraham-Cambridge-CB2-4AT-U-K-",{"title":1669},{"EN":1670},"The Babraham Institute, Babraham Research Campus, Babraham, Cambridge CB2 4AT, U.K.",{"openalex":1672,"orcid":1674,"title":1676},{"VOID":1673},"A5022328608",{"VOID":1675},"https:\u002F\u002Forcid.org\u002F0000-0002-2771-3487",{"EN":1677},"Len Stephens",{"id":1679,"sortIndex":36,"researcher":26,"roles":1680,"affiliations":1681,"properties":1688},"b903537e-0505-401b-807a-8a8dec16b8ff",[],[1682],{"id":1683,"sortIndex":36,"affiliation":1684,"properties":26},"54298d47-e2fb-4f74-b03d-4c0d156d8509",{"id":1663,"createTime":1664,"updateTime":1665,"relativeEntities":1685,"slug":1667,"properties":1686,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1687},{"EN":1670},{"openalex":1689,"orcid":1691,"title":1693},{"VOID":1690},"A5024560049",{"VOID":1692},"https:\u002F\u002Forcid.org\u002F0000-0002-6979-0464",{"EN":1694},"Phillip T. Hawkins",{"id":1696,"sortIndex":115,"researcher":26,"roles":1697,"affiliations":1698,"properties":1705},"f21f7081-4a34-4c70-a140-69b696645554",[],[1699],{"id":1700,"sortIndex":36,"affiliation":1701,"properties":26},"185d7ed3-6b36-4593-9511-f08592850d70",{"id":1663,"createTime":1664,"updateTime":1665,"relativeEntities":1702,"slug":1667,"properties":1703,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":1704},{"EN":1670},{"openalex":1706,"orcid":1708,"title":1710},{"VOID":1707},"A5073316451",{"VOID":1709},"https:\u002F\u002Forcid.org\u002F0000-0002-7394-6660",{"EN":1711},"Karen E. 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When activated by ATP depletion, it switches off ATP-consuming processes, while switching on catabolic pathways that generate ATP. AMPK exists as heterotrimeric complexes comprising catalytic α subunits and regulatory β and γ subunits, each of which occurs as multiple isoforms. Rising AMP and falling ATP, brought about by various types of cellular stress (including exercise in skeletal muscle), stimulate the system in an ultrasensitive manner. Acetyl-CoA carboxylase (ACC) exists in mammals as two isoforms, termed ACC-1 and ACC-2 (also known as ACC-α and ACC-β). AMPK phosphorylates and inactivates both isoforms at the equivalent site. Knockout mice, and other approaches, suggest that the malonyl-CoA produced by ACC-2 is exclusively involved in regulation of fatty acid oxidation, whereas that produced by ACC-1 is utilized in fatty acid synthesis. Activation of AMPK by cellular stress or exercise therefore switches on fatty acid oxidation (via phosphorylation of ACC-2) while switching off fatty acid synthesis (via phosphorylation of ACC-1). The Drosophila melanogaster genome contains single genes encoding homologues of the α, β and γ subunits of AMPK (DmAMPK) and of ACC (DmACC). Studies in a Drosophila embryonal cell line show that DmAMPK is activated by stresses that cause ATP depletion (oligomycin, hypoxia or glucose deprivation) and that this is associated with phosphorylation of the site on DmACC equivalent to the AMPK sites on mammalian ACC-1 and ACC-2. This is abolished when expression of DmAMPK is ablated using an RNA interference approach, proving that DmAMPK is necessary for phosphorylation of DmACC in response to ATP depletion.\u003C\u002Fjats:p>","\u003Cjats:p>Protein kinase được kích hoạt AMP (AMPK) là một cảm biến của năng lượng tế bào và là một ‘công tắc chuyển hóa chính’. Khi được kích hoạt do sự suy giảm ATP, AMPK ngừng các quá trình tiêu tốn ATP, trong khi kích hoạt các con đường dị hóa tạo ra ATP. AMPK tồn tại dưới dạng các phức hợp heterotrimeric bao gồm các đơn vị α xúc tác và các đơn vị β và γ điều hòa, mỗi đơn vị có nhiều isoform khác nhau. Sự gia tăng AMP và sự giảm ATP, do nhiều loại căng thẳng tế bào gây ra (bao gồm cả hoạt động thể chất trong cơ bắp), kích thích hệ thống một cách cực nhạy. Acetyl-CoA carboxylase (ACC) tồn tại ở động vật có vú dưới hai isoform, được gọi là ACC-1 và ACC-2 (còn được biết đến là ACC-α và ACC-β). AMPK phosphoryl hóa và bất hoạt cả hai isoform tại vị trí tương ứng. Các con chuột knockout và các phương pháp khác cho thấy rằng malonyl-CoA được sản xuất bởi ACC-2 chỉ được liên quan đến việc điều chỉnh oxy hóa axit béo, trong khi malonyl-CoA được sản xuất bởi ACC-1 được sử dụng trong tổng hợp axit béo. Sự kích hoạt AMPK bởi căng thẳng tế bào hoặc hoạt động thể chất do đó kích hoạt quá trình oxy hóa axit béo (thông qua phosphoryl hóa ACC-2) trong khi ngừng tổng hợp axit béo (thông qua phosphoryl hóa ACC-1). Bộ gen của Drosophila melanogaster chứa các gen đơn lẻ mã hóa các đồng loại của các đơn vị α, β và γ của AMPK (DmAMPK) và của ACC (DmACC). Các nghiên cứu trong một dòng tế bào phôi của Drosophila cho thấy rằng DmAMPK được kích hoạt bởi các căng thẳng gây ra sự suy giảm ATP (oligomycin, thiếu oxy hoặc thiếu glucose) và điều này liên quan đến phosphoryl hóa tại vị trí trên DmACC tương ứng với các vị trí AMPK trên ACC-1 và ACC-2 ở động vật có vú. Việc này bị triệt tiêu khi sự biểu hiện của DmAMPK bị loại bỏ bằng cách sử dụng phương pháp can thiệp RNA, chứng minh rằng DmAMPK là cần thiết cho sự phosphoryl hóa của DmACC để đáp ứng với sự suy giảm ATP.\u003C\u002Fjats:p>",{"EN":2121,"VI":2122},"Regulation of fatty acid synthesis and oxidation by the AMP-activated protein kinase","Quản lý tổng hợp và oxy hóa axit béo bởi protein kinase được kích hoạt AMP",{"VOID":2124},"12440973",{"VOID":2126},"10.1042\u002Fbst0301064",[102],[101],"https:\u002F\u002Fportlandpress.com\u002Fbiochemsoctrans\u002Farticle\u002F30\u002F6\u002F1064\u002F63780\u002FRegulation-of-fatty-acid-synthesis-and-oxidation",[2131,2152],{"id":2132,"sortIndex":115,"researcher":26,"roles":2133,"affiliations":2134,"properties":2145},"b7297909-e05d-4f93-a473-7c77cf7eeb62",[],[2135],{"id":2136,"sortIndex":36,"affiliation":2137,"properties":26},"248d866a-2575-4551-98f5-db7634c0a179",{"id":2138,"createTime":2139,"updateTime":2139,"relativeEntities":2140,"slug":2141,"properties":2142,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"fba060b9-7381-4ae2-9482-6b5d4f4f51e0","2024-09-20T09:10:38.130+00:00",[],"Division-of-Molecular-Physiology-School-of-Life-Sciences-Dundee-University-Dundee-U-K-and-Wellcome-Trust-Biocentre-Dundee-University-Dundee-U-K-",{"title":2143},{"EN":2144},"Division of Molecular Physiology, School of Life Sciences, Dundee University, Dundee, U.K., and Wellcome Trust Biocentre, Dundee University, Dundee, U.K.",{"openalex":2146,"orcid":2148,"title":2150},{"VOID":2147},"A5038112359",{"VOID":2149},"https:\u002F\u002Forcid.org\u002F0009-0004-5236-7936",{"EN":2151},"David Pan",{"id":2153,"sortIndex":36,"researcher":26,"roles":2154,"affiliations":2155,"properties":2162},"f2f0328c-8b14-4688-a8f8-3c43800e3a62",[],[2156],{"id":2157,"sortIndex":36,"affiliation":2158,"properties":26},"0ef23c4d-328a-4d65-bf9e-cb1221af8ede",{"id":2138,"createTime":2139,"updateTime":2139,"relativeEntities":2159,"slug":2141,"properties":2160,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2161},{"EN":2144},{"openalex":2163,"orcid":2165,"title":2167},{"VOID":2164},"A5046976143",{"VOID":2166},"https:\u002F\u002Forcid.org\u002F0000-0002-8373-7379",{"EN":2168},"D. Grahame Hardie",{"url":26,"publisher":2170,"properties":2195},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":2171,"slug":663,"properties":2172,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":2178,"manageAffiliations":2179,"indexDatabases":2180,"url":734,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":2173,"issn":2174,"introduce":2175,"eissn":2176,"title":2177},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[2181,2188],{"id":697,"indexDatabase":2182,"url":712,"indexYears":26,"academicFieldIds":2187,"indexDatabaseRanking":26},{"id":699,"createTime":700,"updateTime":701,"relativeEntities":2183,"label":2184,"description":2185,"key":708,"publicationTags":2186,"standard":26},[],{"EN":704,"VI":704},{"VI":706,"EN":707},[710,711],[714],{"id":716,"indexDatabase":2189,"url":729,"indexYears":730,"academicFieldIds":2194,"indexDatabaseRanking":733},{"id":718,"createTime":719,"updateTime":720,"relativeEntities":2190,"label":2191,"description":2192,"key":726,"publicationTags":2193,"standard":26},[],{"EN":723,"VI":723},{"EN":723,"VI":725},[728],[732],{"volume":2196,"pages":2197,"issue":2199},{"VOID":1229},{"VOID":2198},"1064-1070",{"VOID":1233},519,{"total":2200,"publishYear":26,"statisticByYear":2202},{"2012":173,"2013":241,"2014":260,"2015":239,"2016":125,"2017":242,"2018":240,"2019":608,"2020":539,"2021":396,"2022":125,"2023":396,"2024":237},[],{"id":2205,"createTime":2206,"updateTime":2207,"relativeEntities":2208,"slug":2209,"properties":2210,"entityType":755,"verifyStatus":25,"verifyTime":2206,"verifyNote":756,"syncStatus":28,"languages":2227,"translateLanguages":2228,"viewCount":36,"primaryUrl":2229,"fullTextUrl":26,"authors":2230,"publicationType":799,"publisherRelationship":2284,"citationCount":846,"citationInfo":2315,"publishDate":1419,"publishYear":1420,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2317,"isForceReanalyzing":851},"b11b93aa-e4d3-47ad-8ad1-a8b8ac687adf","2024-09-01T06:27:28.805+00:00","2025-02-11T19:12:43.512+00:00",[],"Reactive-oxygen-species-in-oncogenic-transformation",{"mag":2211,"keywords":2213,"openalex":2215,"abstract":2217,"title":2220,"pm":2223,"doi":2225},{"VOID":2212},"2033910705",{"VI":2214},"oxy phản ứng, ung thư, quá trình tế bào, sinh học phân tử, liệu pháp gen",{"VOID":2216},"W2033910705",{"EN":2218,"VI":2219},"\u003Cjats:p>Ever since ROS (reactive oxygen species) were shown to meet the criteria of true signalling molecules, such as regulated production and a specific biological function, many efforts have been made to understand the precise role of ROS. The function of ROS in pathological mechanisms is taking a more and more central role in various fields of biomedical research, including neurobiology, cardiology and cancer. An elevated oxidative status has been found in many types of cancer cells, and the introduction of chemical and enzymological antioxidants can inhibit tumour cell proliferation, pointing to a critical role of ROS in mediating loss of growth control. The present review describes ROS-regulated mechanisms that are associated with cancer and tumour invasiveness. The cellular processes that are linked to these ROS functions are mitogenic signalling and cell motility, while ROS have also been implicated in apoptosis and cellular senescence, two mechanisms regarded as being anti-tumorigenic. This ‘two-faced’ character of free radicals will be discussed and placed in the context of the physiological conditions of the tumour cell, the different molecular backgrounds, and the specific ROS. More detailed understanding of the signalling pathways regulated by ROS in tumour cells will open up new prospects for chemo- or gene-therapeutic interventions.\u003C\u002Fjats:p>","\u003Cjats:p>Kể từ khi các loài oxy phản ứng (ROS) được chứng minh đáp ứng các tiêu chí của các phân tử tín hiệu thực thụ, chẳng hạn như sản xuất được điều tiết và một chức năng sinh học cụ thể, nhiều nỗ lực đã được thực hiện để hiểu rõ vai trò chính xác của ROS. Chức năng của ROS trong các cơ chế bệnh lý đang ngày càng đóng vai trò trung tâm trong nhiều lĩnh vực nghiên cứu y sinh, bao gồm thần kinh học, tim mạch và ung thư. Một trạng thái oxy hóa gia tăng đã được phát hiện trong nhiều loại tế bào ung thư, và việc đưa vào các chất chống oxy hóa hóa học và enzym có thể ức chế sự phát triển của tế bào khối u, chỉ ra vai trò quan trọng của ROS trong việc trung gian mất kiểm soát sự phát triển. Bài đánh giá hiện tại mô tả các cơ chế điều chỉnh bởi ROS có liên quan đến ung thư và sự xâm lấn của khối u. Các quá trình tế bào liên quan đến các chức năng ROS này là tín hiệu phân bào và sự di động của tế bào, trong khi ROS cũng đã được liên quan đến apoptosis và sự lão hóa tế bào, hai cơ chế được coi là có tính chống ung thư. Đặc điểm ‘hai mặt’ này của các gốc tự do sẽ được thảo luận và đặt trong bối cảnh của các điều kiện sinh lý của tế bào khối u, các nền tảng phân tử khác nhau và các loại ROS cụ thể. Hiểu biết sâu hơn về các con đường tín hiệu được điều chỉnh bởi ROS trong các tế bào khối u sẽ mở ra triển vọng mới cho các can thiệp hóa trị hoặc liệu pháp gen.",{"EN":2221,"VI":2222},"Reactive oxygen species in oncogenic transformation","Các loài oxy phản ứng trong quá trình chuyển hóa ung thư",{"VOID":2224},"14641084",{"VOID":2226},"10.1042\u002Fbst0311441",[102],[101],"https:\u002F\u002Fportlandpress.com\u002Fbiochemsoctrans\u002Farticle\u002F31\u002F6\u002F1441\u002F64575\u002FReactive-oxygen-species-in-oncogenic",[2231,2250,2267],{"id":2232,"sortIndex":36,"researcher":26,"roles":2233,"affiliations":2234,"properties":2245},"32f4c7eb-e255-4e35-8855-a8ac0160a3c3",[],[2235],{"id":2236,"sortIndex":36,"affiliation":2237,"properties":26},"5d6bba9f-3016-4a41-9e8f-db355a2ee0ed",{"id":2238,"createTime":2239,"updateTime":2239,"relativeEntities":2240,"slug":2241,"properties":2242,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"6efc7f52-fcd7-45af-9a49-c4808b219e97","2024-09-01T06:27:28.817+00:00",[],"Division-of-Gene-Therapy-and-Interdisciplinary-Clinical-Research-Center-University-of-Ulm-Helmholtzstrasse-8-1-89081-Ulm-Germany",{"title":2243},{"EN":2244},"Division of Gene Therapy and Interdisciplinary Clinical Research Center, University of Ulm, Helmholtzstrasse 8\u002F1, 89081 Ulm, Germany",{"openalex":2246,"title":2248},{"VOID":2247},"A5007985951",{"EN":2249},"Lars Behrend",{"id":2251,"sortIndex":114,"researcher":26,"roles":2252,"affiliations":2253,"properties":2260},"2b746961-9dc7-4e83-a6ec-4e5b7332f566",[],[2254],{"id":2255,"sortIndex":36,"affiliation":2256,"properties":26},"a9f98ce3-6547-43ce-ad6c-990d3c843249",{"id":2238,"createTime":2239,"updateTime":2239,"relativeEntities":2257,"slug":2241,"properties":2258,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2259},{"EN":2244},{"openalex":2261,"orcid":2263,"title":2265},{"VOID":2262},"A5044483462",{"VOID":2264},"https:\u002F\u002Forcid.org\u002F0000-0003-2821-0387",{"EN":2266},"Ralf M. Zwacka",{"id":2268,"sortIndex":115,"researcher":26,"roles":2269,"affiliations":2270,"properties":2277},"ba38a2b3-d8a1-4523-878c-e1ae07849ec4",[],[2271],{"id":2272,"sortIndex":36,"affiliation":2273,"properties":26},"de0e3bcd-62db-46fa-86e9-eed73b0144dc",{"id":2238,"createTime":2239,"updateTime":2239,"relativeEntities":2274,"slug":2241,"properties":2275,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2276},{"EN":2244},{"openalex":2278,"orcid":2280,"title":2282},{"VOID":2279},"A5071988751",{"VOID":2281},"https:\u002F\u002Forcid.org\u002F0000-0001-8991-8157",{"EN":2283},"George I. Henderson",{"url":26,"publisher":2285,"properties":2310},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":2286,"slug":663,"properties":2287,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":2293,"manageAffiliations":2294,"indexDatabases":2295,"url":734,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":2288,"issn":2289,"introduce":2290,"eissn":2291,"title":2292},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[2296,2303],{"id":697,"indexDatabase":2297,"url":712,"indexYears":26,"academicFieldIds":2302,"indexDatabaseRanking":26},{"id":699,"createTime":700,"updateTime":701,"relativeEntities":2298,"label":2299,"description":2300,"key":708,"publicationTags":2301,"standard":26},[],{"EN":704,"VI":704},{"VI":706,"EN":707},[710,711],[714],{"id":716,"indexDatabase":2304,"url":729,"indexYears":730,"academicFieldIds":2309,"indexDatabaseRanking":733},{"id":718,"createTime":719,"updateTime":720,"relativeEntities":2305,"label":2306,"description":2307,"key":726,"publicationTags":2308,"standard":26},[],{"EN":723,"VI":723},{"EN":723,"VI":725},[728],[732],{"volume":2311,"pages":2312,"issue":2314},{"VOID":1412},{"VOID":2313},"1441-1444",{"VOID":1233},{"total":846,"publishYear":26,"statisticByYear":2316},{"2012":397,"2013":159,"2014":257,"2015":125,"2016":240,"2017":222,"2018":241,"2019":53,"2020":255,"2021":173,"2022":241,"2023":238,"2024":158},[],{"id":2319,"createTime":2320,"updateTime":2321,"relativeEntities":2322,"slug":2323,"properties":2324,"entityType":755,"verifyStatus":25,"verifyTime":2320,"verifyNote":756,"syncStatus":28,"languages":2340,"translateLanguages":2341,"viewCount":36,"primaryUrl":2342,"fullTextUrl":26,"authors":2343,"publicationType":799,"publisherRelationship":2366,"citationCount":2399,"citationInfo":2400,"publishDate":2402,"publishYear":2403,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2404,"isForceReanalyzing":851},"f88b1384-869b-4ea8-8a0a-a2ede76e490a","2025-01-29T10:23:59.050+00:00","2025-02-11T19:13:40.987+00:00",[],"Oxidative-stress-the-vulnerable-%CE%B2-cell",{"mag":2325,"keywords":2327,"openalex":2328,"abstract":2330,"title":2333,"pm":2336,"doi":2338},{"VOID":2326},"1994567337",{"VI":862},{"VOID":2329},"W1994567337",{"EN":2331,"VI":2332},"\u003Cjats:p>Antioxidative defence mechanisms of pancreatic β-cells are particularly weak and can be overwhelmed by redox imbalance arising from overproduction of reactive oxygen and reactive nitrogen species. The consequences of this redox imbalance are lipid peroxidation, oxidation of proteins, DNA damage and interference of reactive species with signal transduction pathways, which contribute significantly to β-cell dysfunction and death in Type 1 and Type 2 diabetes mellitus. Reactive oxygen species, superoxide radicals (O2•−), hydrogen peroxide (H2O2) and, in a final iron-catalysed reaction step, the most reactive and toxic hydroxyl radicals (OH•) are produced during both pro-inflammatory cytokine-mediated β-cell attack in Type 1 diabetes and glucolipotoxicity-mediated β-cell dysfunction in Type 2 diabetes. In combination with NO•, which is toxic in itself, as well as through its reaction with the O2•− and subsequent formation of peroxynitrite, reactive species play a central role in β-cell death during the deterioration of glucose tolerance in the development of diabetes.\u003C\u002Fjats:p>","\u003Cjats:p>Các cơ chế phòng vệ chống oxy hóa của tế bào β tụy đặc biệt yếu và có thể bị quá tải bởi sự mất cân bằng redox phát sinh từ việc sản xuất quá mức các loại oxy phản ứng và các loài nitơ phản ứng. Những hậu quả của sự mất cân bằng redox này bao gồm quá trình peroxy hóa lipid, oxy hóa protein, tổn thương DNA và sự can thiệp của các loài phản ứng với các con đường truyền tín hiệu, điều này góp phần đáng kể vào sự suy giảm và chết tế bào β trong bệnh tiểu đường loại 1 và loại 2. Các loại oxy phản ứng, các gốc superoxide (O2•−), hydrogen peroxide (H2O2) và, trong giai đoạn phản ứng cuối cùng được xúc tác bởi sắt, các gốc hydroxyl phản ứng mạnh nhất và độc hại nhất (OH•) được sản xuất trong cả hai quá trình tấn công tế bào β do cytokine gây viêm trong bệnh tiểu đường loại 1 và sự suy giảm chức năng tế bào β do glucolipotoxicity trong bệnh tiểu đường loại 2. Kết hợp với NO•, vốn độc hại tự nó, cũng như thông qua phản ứng của nó với O2•− và hình thành sau đó peroxynitrite, các loài phản ứng đóng vai trò trung tâm trong sự chết của tế bào β trong quá trình suy giảm dung nạp glucose khi phát triển bệnh tiểu đường.\u003C\u002Fjats:p>",{"EN":2334,"VI":2335},"Oxidative stress: the vulnerable β-cell","Căng thẳng oxy hóa: tế bào β dễ tổn thương",{"VOID":2337},"18481954",{"VOID":2339},"10.1042\u002Fbst0360343",[102],[101],"https:\u002F\u002Fportlandpress.com\u002Fbiochemsoctrans\u002Farticle\u002F36\u002F3\u002F343\u002F66120\u002FOxidative-stress-the-vulnerable-cell",[2344],{"id":2345,"sortIndex":36,"researcher":26,"roles":2346,"affiliations":2347,"properties":2359},"3eafb9a8-c825-4224-8074-7054e04f5d96",[],[2348],{"id":2349,"sortIndex":36,"affiliation":2350,"properties":26},"df42aa5d-551d-49c4-8324-a5b6b47dbb91",{"id":2351,"createTime":2352,"updateTime":2353,"relativeEntities":2354,"slug":2355,"properties":2356,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"87b02192-822a-4493-9cbf-b4cd210004a9","2024-04-20T08:54:08.788+00:00","2025-01-29T10:23:59.086+00:00",[],"Institute-of-Clinical-Biochemistry-Hannover-Medical-School-30625-Hannover-Germany",{"title":2357},{"EN":2358},"Institute of Clinical Biochemistry, Hannover Medical School, 30625, Hannover, Germany",{"openalex":2360,"orcid":2362,"title":2364},{"VOID":2361},"A5043148796",{"VOID":2363},"https:\u002F\u002Forcid.org\u002F0000-0003-2125-8193",{"EN":2365},"Sigurd Lenzen",{"url":26,"publisher":2367,"properties":2392},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":2368,"slug":663,"properties":2369,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":2375,"manageAffiliations":2376,"indexDatabases":2377,"url":734,"thumbnailPath":26,"statistic":26,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":2370,"issn":2371,"introduce":2372,"eissn":2373,"title":2374},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":674},[],[],[2378,2385],{"id":697,"indexDatabase":2379,"url":712,"indexYears":26,"academicFieldIds":2384,"indexDatabaseRanking":26},{"id":699,"createTime":700,"updateTime":701,"relativeEntities":2380,"label":2381,"description":2382,"key":708,"publicationTags":2383,"standard":26},[],{"EN":704,"VI":704},{"VI":706,"EN":707},[710,711],[714],{"id":716,"indexDatabase":2386,"url":729,"indexYears":730,"academicFieldIds":2391,"indexDatabaseRanking":733},{"id":718,"createTime":719,"updateTime":720,"relativeEntities":2387,"label":2388,"description":2389,"key":726,"publicationTags":2390,"standard":26},[],{"EN":723,"VI":723},{"EN":723,"VI":725},[728],[732],{"volume":2393,"pages":2395,"issue":2397},{"VOID":2394},"36",{"VOID":2396},"343-347",{"VOID":2398},"3",495,{"total":2399,"publishYear":26,"statisticByYear":2401},{"2012":286,"2013":159,"2014":285,"2015":397,"2016":285,"2017":398,"2018":79,"2019":173,"2020":396,"2021":48,"2022":237,"2023":260,"2024":516},"2008-06-01",2008,[2405,2409,2413,2416,2420,2424,2428,2432,2436,2440,2444,2448,2452,2456,2460,2464,2468,2472,2476,2480,2484,2488,2492,2496,2500,2504,2508,2512,2516,2520,2524],{"id":26,"text":2406,"url":26,"identifiers":2407},"Lenzen, 1996, Low antioxidant enzyme gene expression in pancreatic islets compared with various other mouse tissues, Free Radical Biol. 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