Document Detail


Inhibitor specificity of recombinant and endogenous caspase-9.
MedLine Citation:
PMID:  12067274     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Apoptosis triggered through the intrinsic pathway by radiation and anti-neoplastic drugs is initiated by the activation of caspase-9. To elucidate control mechanisms in this pathway we used a range of synthetic and natural reagents. The inhibitory potency of acetyl-Asp-Glu-Val-Asp-aldehyde ('Ac-DEVD-CHO'), benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone ('Z-VAD-FMK') and the endogenous caspase inhibitor X-chromosome-linked inhibitor of apoptosis protein ('XIAP') against recombinant caspase-9 were predictive of the efficacy of these compounds in a cell-free system. However, the viral proteins CrmA and p35, although potent inhibitors of recombinant caspase-9, had almost no ability to block caspase-9 in this system. These findings were also mirrored in cell expression studies. We hypothesize that the viral inhibitors CrmA and p35 are excluded from reacting productively with the natural form of active caspase-9 in vivo, making the potency of inhibitors highly context-dependent. This is supported by survival data from a mouse model of apoptosis driven by Sindbis virus expressing either p35 or a catalytic mutant of caspase-9. These results consolidate previous findings that CrmA is a potent inhibitor of caspase-9 in vitro, yet fails to block caspase-9-mediated cell death.
Authors:
Ciara A Ryan; Henning R Stennicke; Victor E Nava; Jennifer B Burch; J Marie Hardwick; Guy S Salvesen
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Biochemical journal     Volume:  366     ISSN:  0264-6021     ISO Abbreviation:  Biochem. J.     Publication Date:  2002 Sep 
Date Detail:
Created Date:  2002-08-21     Completed Date:  2002-10-17     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  2984726R     Medline TA:  Biochem J     Country:  England    
Other Details:
Languages:  eng     Pagination:  595-601     Citation Subset:  IM    
Affiliation:
Program for Apoptosis and Cell Death Research, The Burnham Institute, 10901 North, Torrey Pines Road, La Jolla, CA 92037, USA.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Chloromethyl Ketones / pharmacology
Apoptosis / drug effects
Caspase 9
Caspases / antagonists & inhibitors*
Cell Line
Cysteine Proteinase Inhibitors / pharmacology*
Humans
Kidney
Kinetics
Oligopeptides / pharmacology
Proteins / physiology
Recombinant Proteins / antagonists & inhibitors
Substrate Specificity
X Chromosome
X-Linked Inhibitor of Apoptosis Protein
Zinc Fingers
Grant Support
ID/Acronym/Agency:
AG15402/AG/NIA NIH HHS; NS34175/NS/NINDS NIH HHS; NS37878/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Amino Acid Chloromethyl Ketones; 0/Cysteine Proteinase Inhibitors; 0/Oligopeptides; 0/Proteins; 0/Recombinant Proteins; 0/X-Linked Inhibitor of Apoptosis Protein; 0/XIAP protein, human; 0/acetyl-aspartyl-glutamyl-valyl-aspartal; 0/benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; EC 3.4.22.-/CASP9 protein, human; EC 3.4.22.-/Casp9 protein, mouse; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Caspases
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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