14-3-3σ is a p53-regulated inhibitor of G2/M progression

被引：1283

作者：

Hermeking, H ^{[1
]}

Lengauer, C

Polyak, K

He, TC

Zhang, L

Thiagalingam, S

Kinzler, KW

Vogelstein, B

机构：

[1] Johns Hopkins Univ, Sch Med, Johns Hopkins Oncol Ctr, Baltimore, MD 21231 USA

[2] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21231 USA

来源：

MOLECULAR CELL | 1997年 / 1卷 / 01期

关键词：

D O I：

10.1016/S1097-2765(00)80002-7

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

Exposure of colorectal cancer (CRC) cells to ionizing radiation results in a cell-cycle arrest in G1 and G2. The G1 arrest is due to p53-mediated induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1/SDI1), but the basis for the G2 arrest is unknown. Through a quantitative analysis of gene expression patterns in CRC cell lines, we have discovered that 14-3-3 sigma is strongly induced by gamma irradiation and other DNA-damaging agents. The induction of 14-3-3 sigma is mediated by a p53-responsive element located 1.8 kb upstream of its transcription start site. Exogenous introduction of 14-3-3 sigma into cycling cells results in a G2 arrest. As the fission yeast 14-3-3 homologs rad24 and rad25 mediate similar checkpoint effects, these results document a molecular mechanism for G2/M control that is conserved throughout eukaryotic evolution and regulated in human cells by p53.

引用

页码：3 / 11

页数：9

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