Cell growth arrest and induction of cyclin-dependent kinase inhibitor p21(WAF1/CIP1) mediated by STAT1

被引：737

作者：

Chin, YE ^{[1
]}

Kitagawa, M ^{[1
]}

Su, WCS ^{[1
]}

You, ZH ^{[1
]}

Iwamoto, Y ^{[1
]}

Fu, XY ^{[1
]}

机构：

[1] YALE UNIV,SCH MED,DEPT PATHOL,NEW HAVEN,CT 06520

来源：

SCIENCE | 1996年 / 272卷 / 5262期

关键词：

D O I：

10.1126/science.272.5262.719

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Signal transducers and activators of transcription (STAT) proteins can be conditionally activated in response to epidermal growth factor (EGF) and interferon (IFN)-gamma. STAT activation was correlated with cell growth inhibition in response to EGF and IFN-gamma. Activated STAT proteins' specifically recognized the conserved STAT-responsive elements in the promoter of the gene encoding the cyclin-dependent kinase (CDK) inhibitor p21(WAF1/CIP1) and regulated the induction of p21 messenger RNA. IFN-gamma did not inhibit the growth of U3A cells, which are deficient in STAT1, but did inhibit the growth of U3A cells into which STAT1 alpha was reintroduced. Thus, STAT1 protein is essential for cell growth suppression in response to IFN-gamma. The STAT signaling pathway appears to negatively regulate the cell cycle by inducing CDK inhibitors in response to cytokines.

引用

页码：719 / 722

页数：4

共 44 条

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