Egr-1 inhibits apoptosis during the UV response: correlation of cell survival with Egr-1 phosphorylation

被引：58

作者：

Huang, RP

Fan, Y

deBelle, I

Ni, ZY

Matheny, W

Adamson, ED

机构：

[1] Burnham Inst, La Jolla, CA 92037 USA

[2] NW Hosp, Seattle, WA 98125 USA

来源：

CELL DEATH AND DIFFERENTIATION | 1998年 / 5卷 / 01期

关键词：

early growth response-1 transcription factor; UV-C response; clonogenicity; phosphorylation; HT1080 fibrosarcoma cells; Egr-1 response element; transactivation;

D O I：

10.1038/sj.cdd.4400322

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：

UV irradiation of normal or immortalized cells induces a rapid increase in the expression of several transcription factors and is thought to serve a protective function. The human fibrosarcoma cell line, HT1080 clone H4, expresses almost undetectable levels of Egr-1 and does not respond to UV-C irradiation by the induction of Egr-1. The H4 cells are hypersensitive to UV which induces apoptosis and reduces clonogenicity. The introduction of exogenous Egr-1 into H4 (H4E9 and H4E4 cell-lines) confers protection from UV-damage as measured by a number of assays. In both NIH3T3 (with inducible Egr-1) and H4E9 (constitutive Egr-1) cells, UV irradiation gave enhanced transactivation of Egr-1 reporters that correlated with phosphorylated Egr-1. Studies using inhibitors indicated that protein kinase-C and tyrosine kinases are involved in the anti-apoptotic effects of Egr-1 after UV damage. This is the first description of a biological effect of phosphorylated Egr-1.

引用

页码：96 / 106

页数：11

共 45 条

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