Document Detail


Androgen via p21 inhibits tumor necrosis factor alpha-induced JNK activation and apoptosis.
MedLine Citation:
PMID:  19723627     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Fangming Tang; John Kokontis; Yuting Lin; Shutsung Liao; Anning Lin; Jialing Xiang
Related Documents :
20680307 - Tnfα protects cardiac mitochondria independently of its cell surface receptors.
9036957 - Lack of type 2 t cell-independent b cell responses and defect in isotype switching in t...
19174567 - Diffusion tensor anisotropy magnetic resonance imaging: a new tool to assess synovial i...
7891367 - The modulating effects of tumor necrosis factor alpha antibody on ricin-induced oxidati...
25136627 - Abarema cochliacarpos extract decreases the inflammatory process and skeletal muscle in...
11345837 - Expression of decorin, transforming growth factor-beta 1, tissue inhibitor metalloprote...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-09-01
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  284     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-11-16     Completed Date:  2009-12-14     Revised Date:  2014-09-11    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  32353-8     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Alleles
Androgens / metabolism*
Apoptosis
Cell Line, Tumor
Cyclin-Dependent Kinase Inhibitor p21 / metabolism*
Enzyme Activation
Gene Expression Regulation, Neoplastic*
Humans
MAP Kinase Kinase 4 / metabolism*
Male
Models, Biological
Prostatic Neoplasms / metabolism
Receptors, Androgen / metabolism
Transcription, Genetic
Tumor Necrosis Factor-alpha / metabolism*
Grant Support
ID/Acronym/Agency:
CA090516/CA/NCI NIH HHS; CA128114/CA/NCI NIH HHS; ES015868/ES/NIEHS NIH HHS; GM71409/GM/NIGMS NIH HHS; R01 CA058073/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/AR protein, human; 0/Androgens; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Receptors, Androgen; 0/Tumor Necrosis Factor-alpha; EC 2.7.12.2/MAP Kinase Kinase 4
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Atypical responsiveness of the orphan receptor GPR55 to cannabinoid ligands.
Next Document:  Deletion of the chloride transporter slc26a7 causes distal renal tubular acidosis and impairs gastri...