KLF6 degradation after apoptotic DNA damage

被引：30

作者：

Banck, Michaela S.

Beaven, Simon W.

Narla, Goutham

Walsh, Martin J.

Friedman, Scott L.

Beutler, Andreas S.

机构：

[1] CUNY Mt Sinai Sch Med, Dept Med, Div Hematol Oncol, New York, NY 10029 USA

[2] CUNY Mt Sinai Sch Med, Dept Human Genet, New York, NY 10029 USA

[3] CUNY Mt Sinai Sch Med, Dept Pediat, New York, NY 10029 USA

[4] CUNY Mt Sinai Sch Med, Div Liver Dis, New York, NY 10029 USA

来源：

FEBS LETTERS | 2006年 / 580卷 / 30期

关键词：

Kruppel-like factor; KLF6; DNA-damage; apoptosis; chemosensitivity; proteasomal degradation; ubiquitin; cancer cells; carcinogenesis;

D O I：

10.1016/j.febslet.2006.10.077

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Kruppel-like factor 6 (KLF6) is a cancer gene (www.sanger.ac.uk/genetics/CGP/Census/). Here, we demonstrate that KLF6 protein is rapidly degraded when apoptosis is induced via the intrinsic pathway by cisplatin, adriamycin, or UVB irradiation in multiple cell lines (HCT116, SW40, HepG2, PO-M, Skov3, NIH-3T3, 293T, GM09706, and MEF, IMR90). KLF6 degradation occurred in the presence or absence of p53, was associated with ubiquitination, mediated by the proteasome (half-life 16 min, unstimulated), and independent of caspases and calpain. KLF6 was unchanged by apoptosis via the extrinsic/death-receptor pathway. Deregulation of KLF6 stability may alter its tumor suppressor function and/or the response of tumors to chemotherapeutics. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

收藏

页码：6981 / 6986

页数：6

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