کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10771956 | 1050845 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Downregulation of β1,4-galactosyltransferase 1 inhibits CDK11p58-mediated apoptosis induced by cycloheximide
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Cyclin-dependent kinase 11 (CDK11; also named PITSLRE) is part of the large family of p34cdc2-related kinases whose functions appear to be linked with cell cycle progression, tumorigenesis, and apoptotic signaling. The mechanism that CDK11p58 induces apoptosis is not clear. Some evidences suggested β1,4-galactosyltransferase 1 (β1,4-GT 1) might participate in apoptosis induced by CDK11p58. In this study, we demonstrated that ectopically expressed β1,4-GT 1 increased CDK11p58-mediated apoptosis induced by cycloheximide (CHX). In contrast, RNAi-mediated knockdown of β1,4-GT 1 effectively inhibited apoptosis induced by CHX in CDK11p58-overexpressing cells. For example, the cell morphological and nuclear changes were reduced; the loss of cell viability was prevented and the number of cells in sub-G1 phase was decreased. Knock down of β1,4-GT 1 also inhibited the release of cytochrome c from mitochondria and caspase-3 processing. Therefore, the cleavage of CDK11p58 by caspase-3 was reduced. We proposed that β1,4-GT 1 might contribute to the pro-apoptotic effect of CDK11p58. This may represent a new mechanism of β1,4-GT 1 in CHX-induced apoptosis of CDK11p58-overexpressing cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 327, Issue 2, 11 February 2005, Pages 628-636
Journal: Biochemical and Biophysical Research Communications - Volume 327, Issue 2, 11 February 2005, Pages 628-636
نویسندگان
Zejuan Li, Hanzhou Wang, Hongliang Zong, Qing Sun, Xiangfei Kong, Jianhai Jiang, Jianxin Gu,