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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kokontis, John Lin, Yuting Liao, Shutsung Xiang, Jialing Lin, Anning Tang, Fangming |
| Description | Author Affiliation: Tang F ( Ben May Department for Cancer Research, University of Chicago, Chicago, Illinois 60637, USA.) |
| Abstract | The male hormone androgen is a growth/survival factor for its target tissues or organs. Yet, the underlying mechanism is incompletely understood. Here, we report that androgen via p21 inhibits tumor necrosis factor alpha-induced JNK activation and apoptosis. Inhibition by androgen requires the transcription activity of androgen receptor (AR) and de novo protein synthesis. Androgen.AR induces expression of p21 that in turn inhibits tumor necrosis factor alpha-induced JNK and apoptosis. Furthermore, genetic interruption of p21 alleles abolishes the inhibition by androgen. Our results reveal a novel cross-talk between androgen x AR and JNK, thereby providing a molecular mechanism underlying the survival function of androgen. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 47 |
| Volume Number | 284 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2009-11-20 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Androgens Metabolism Cyclin-Dependent Kinase Inhibitor P21 Gene Expression Regulation, Neoplastic MAP Kinase Kinase 4 Tumor Necrosis Factor-alpha Alleles Apoptosis Cell Line, Tumor Enzyme Activation Models, Biological Prostatic Neoplasms Receptors, Androgen Transcription, Genetic Research Support, N.I.H., Extramural Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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