ASK1-Signaling promotes c-Myc protein stability during apoptosis

被引：30

作者：

Noguchi, K

Kokubu, A

Kitanaka, C

Ichijo, H

Kuchino, Y

机构：

[1] Natl Inst Infect Dis, Dept Bioact Mol, Shinjuku Ku, Tokyo 1628640, Japan

[2] Natl Canc Ctr, Res Inst, Div Biophys, Tokyo 1040045, Japan

[3] Tokyo Med & Dent Univ, Grad Sch, Dept Cell Signaling, Bunkyo Ku, Tokyo 1138549, Japan

[4] CREST, Kawaguchi, Saitama 3320012, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 281卷 / 05期

关键词：

D O I：

10.1006/bbrc.2001.4498

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：

We previously reported that JNK is involved in the regulation of c-Myc-mediated apoptosis triggered by UV irradiation and anticancer drug treatment. Here we show that ASK1 is an upstream regulator for c-Myc-mediated apoptosis triggered by UV, and we found a direct role for Ser-62 and Ser-71 in the regulation of protein stability and function of c-Myc. The ASK1 JNK pathway enhanced the protein stability of c-Myc through phosphorylation at Ser-62 and Ser-71, which was required for c-Myc-dependent apoptosis by ASK1-signaling. Interestingly, ASK1-signaling attenuated the degradation of ubiquitinated c-Myc without affecting the ubiquitination process. Together, these findings indicate that the ASK1-JNK pathway promotes the proapoptotic activity of c-Myc by modulating c-Myc protein stability through phosphorylation at Ser-62 and Ser-71. (C) 2001 Academic Press.

引用

页码：1313 / 1320

页数：8

共 34 条

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