Document Detail

Role of Src-specific phosphorylation site on focal adhesion kinase for senescence-associated apoptosis resistance.
MedLine Citation:
PMID:  16523241     Owner:  NLM     Status:  MEDLINE    
A decreased apoptotic response toward noxious stress is an issuing characteristic of the aging phenotype. Hydrogen peroxide or staurosporine induced apoptosis readily in young cells but not in senescent cells. We showed that focal adhesion kinase (FAK) expression and its phosphorylation at Tyr397, autophosphorylation site for focal adhesion formation, and Tyr577, Src-dependent phosphorylation site, were both increased in senescent cells. Moreover, FAK was inactivated proteolytically by apoptotic stimuli in young cells, but not in senescent cells. In addition, senescent cells whose FAK expression was downregulated by siRNA showed the increased level of apoptosis by staurosporine treatment via caspase-3 activation but not by hydrogen peroxide treatment. Interestingly dephosphorylation at Tyr577 of FAK by PP2 treatment, Src-family kinase inhibitor, induced the apoptosis by staurosporine in senescent cells but dephosphorylation at Tyr397 by downregulation of caveolin-1 was not affected. These data suggest that FAK might differently regulate apoptosis and focal adhesion formation through site-specific tyrosine phosphorylation in senescent cells.
S J Ryu; K A Cho; Y S Oh; S C Park
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Apoptosis : an international journal on programmed cell death     Volume:  11     ISSN:  1360-8185     ISO Abbreviation:  Apoptosis     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-05-04     Completed Date:  2006-12-11     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9712129     Medline TA:  Apoptosis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  303-13     Citation Subset:  IM    
Department of Biochemistry and Molecular Biology, The Aging and Apoptosis Research Center, Seoul National University College of Medicine, Seoul, S. Korea.
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MeSH Terms
Apoptosis / physiology*
Caspase 3 / metabolism
Cell Aging*
Cell Cycle
Cells, Cultured
Collagen Type XI / metabolism
Enzyme Activation
Enzyme Inhibitors / pharmacology
Fibroblasts / cytology,  drug effects,  physiology
Focal Adhesion Protein-Tyrosine Kinases / genetics,  metabolism*
Hydrogen Peroxide / pharmacology
Oxidants / pharmacology
RNA, Small Interfering / metabolism
Staurosporine / pharmacology
Tyrosine / metabolism
src-Family Kinases / antagonists & inhibitors,  metabolism*
Reg. No./Substance:
0/COL11A2 protein, human; 0/Collagen Type XI; 0/Enzyme Inhibitors; 0/Oxidants; 0/RNA, Small Interfering; 55520-40-6/Tyrosine; 62996-74-1/Staurosporine; 7722-84-1/Hydrogen Peroxide; EC Adhesion Protein-Tyrosine Kinases; EC Kinases; EC 3.4.22.-/Caspase 3

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

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