Document Detail

Gadd45b mediates Fas-induced apoptosis by enhancing the interaction between p38 and retinoblastoma tumor suppressor.
MedLine Citation:
PMID:  20558744     Owner:  NLM     Status:  MEDLINE    
Gadd45b has been known as a positive mediator of apoptosis induced by certain cytokines and oncogenes. Here, we identified Gadd45b as an effector of Fas-induced apoptosis and found that p38-mediated Rb hyperphosphorylation is one of the mechanisms of Fas-induced apoptosis in murine hepatocyte AML12 cells. Gadd45b has been shown to activate p38 through its physical interaction with MTK1 and induce apoptosis. However, in this study, we have showed that the function of Gadd45b during Fas-induced apoptosis in AML12 cells is different from that reported in previous studies. Depletion of Gadd45b expression did not inhibit the phosphorylation of p38, but it suppressed p38-mediated Rb phosphorylation and apoptosis in response to Fas stimulation by reducing the interaction between p38 and Rb. Ectopic expression of Gadd45b was sufficient to enhance this interaction. These findings suggest that Gadd45b mediates p38-induced Rb phosphorylation by enhancing the interaction between p38 and Rb during Fas-induced apoptosis in murine hepatocytes.
Hee Jun Cho; Sun-Mi Park; Eun Mi Hwang; Kyoung Eun Baek; In-Kyu Kim; In-Koo Nam; Min-Ju Im; Seung-Ho Park; Seran Bae; Jae-Yong Park; Jiyun Yoo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-17
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  285     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-09     Completed Date:  2010-08-30     Revised Date:  2011-08-25    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  25500-5     Citation Subset:  IM    
Department of Microbiology/Research Institute of Life Science, College of Natural Sciences, Gyeongsang National University, Jinju 660-701, Korea.
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MeSH Terms
Antigens, CD95 / antagonists & inhibitors,  metabolism*
Antigens, Differentiation / metabolism*
Apoptosis / drug effects
Cell Line
Cell Line, Tumor
Enzyme Inhibitors / pharmacology
Hela Cells
Imidazoles / pharmacology
In Situ Nick-End Labeling
Protein Binding / genetics,  physiology
Pyridines / pharmacology
RNA Interference
Retinoblastoma Protein / metabolism*
Reverse Transcriptase Polymerase Chain Reaction
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism*
Reg. No./Substance:
0/Antigens, CD95; 0/Antigens, Differentiation; 0/Enzyme Inhibitors; 0/Gadd45b protein, mouse; 0/Imidazoles; 0/Pyridines; 0/Retinoblastoma Protein; 0/SB 203580; EC Mitogen-Activated Protein Kinases

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