期刊
FEBS LETTERS
卷 538, 期 1-3, 页码 41-47出版社
WILEY
DOI: 10.1016/S0014-5793(03)00131-5
关键词
apoptosis; Bcl-xL; Bcl2; 2-methoxyestradiol; taxol; Jun kinase
资金
- NCI NIH HHS [CA77328] Funding Source: Medline
Bcl-xL, a close homolog of Bcl2, is an important regulator of apoptosis and is overexpressed in human cancer. Phosphorylation of Bcl-xL can be induced by microtubule-damaging drugs such as taxol or 2-methoxyestradiol (2-ME). By site-directed mutagenesis studies, we have identified that serine 62 is the necessary site for taxol- or 2-ME-induced Bcl-xL phosphorylation in prostate cancer cells. Further studies with the inhibitor of Jun kinase (JNK) and phosphorylation null mutant of Bcl-xL reveal the augmentative role of JNK-mediated Bel-xL phosphorylation in apoptosis of prostate cancer cells. In summary, our studies suggest that the phosphorylation of Bcl-xL by stress response kinase signaling might oppose the antiapoptotic function of Bcl-xL to permit prostate cancer cells to die by apoptosis. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
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