Tác động trái ngược của ERK và JNK-p38 MAP Kinases đối với quá trình Apoptosis

American Association for the Advancement of Science (AAAS) - Tập 270 Số 5240 - Trang 1326-1331 - 1995
Zhengui Xia1, Martin Dickens2, Joël Raingeaud2, Roger J. Davis2, Michael E. Greenberg1
1Z. Xia and M. E. Greenberg are in the Division of Neuroscience, Department of Neurology, Children's Hospital, and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
2M. Dickens, J. Raingeaud, and R. J. Davis are in the Howard Hughes Medical Institute and Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.

Tóm tắt

Apoptosis đóng vai trò quan trọng trong phát triển nơron, và các khuyết tật trong apoptosis có thể là nguyên nhân của nhiều rối loạn thoái hóa thần kinh khác nhau. Để đặc tính hóa các cơ chế phân tử điều chỉnh apoptosis nơron, nghiên cứu đã khám phá các đóng góp vào cái chết tế bào của các thành viên thuộc họ kinase protein (MAP), bao gồm ERK (kinase điều tiết tín hiệu ngoại bào), JNK (c-JUN NH 2 -terminal protein kinase) và p38, sau khi loại bỏ yếu tố tăng trưởng thần kinh (NGF) từ các tế bào pheochromocytoma PC-12 của chuột. Loại bỏ NGF dẫn đến sự kích hoạt kéo dài của enzyme JNK và p38 và ức chế của ERK. Các tác động của các dạng tương tác chi phối hoặc kích hoạt thường xuyên của các thành phần khác nhau trong con đường tín hiệu JNK-p38 và ERK cho thấy việc kích hoạt JNK và p38 cùng với sự ức chế đồng thời của ERK là rất quan trọng để cảm ứng apoptosis trong các tế bào này. Do đó, cân bằng động giữa ERK kích hoạt bởi yếu tố tăng trưởng và các con đường tín hiệu JNK-p38 kích hoạt bởi stress có thể quan trọng trong việc xác định xem tế bào có sống sót hay trải qua apoptosis.

Từ khóa


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