Document Detail


Mediation of cell death by poly(ADP-ribose) polymerase-1.
MedLine Citation:
PMID:  15911329     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Poly(ADP-ribosyl)ation plays an important role in modulating the cellular response to stress. The extent of poly(ADP-ribosyl)ation, chiefly via the activation of the poly(ADP-ribose) polymerase-1 (PARP-1), correlates with the severity of genotoxic stress and this determines the cellular response. Under mild and moderate stress, it plays important roles in DNA processing and it participates in the proinflammatory/cellular defense via transcriptional regulation. However, severe stress following acute neuronal injury causes the overactivation of PARP-1, which results in unregulated poly(ADP-ribose) (PAR) synthesis and widespread neuronal cell death. Previously, this PARP-1-dependent cell death mechanism was manifest solely through necrosis, but apoptotic mechanisms are also evident. Poly(ADP-ribosyl)ation directly induces the nuclear translocation of apoptosis-inducing factor, which results in caspase-independent cell death significant in many neurodegenerative conditions. Further, the hydrolysis of PAR by poly(ADP-ribose) glycohydrolase (PARG) has a protective role, since the accumulation of PAR leads to cell death by apoptosis. Thus, PAR signaling, regulated by PARP-1 and PARG, mediates cell death. Accordingly, modulation of PAR synthesis or degradation through the targeting of PARP-1 or PARG holds particular promise in the treatment of conditions such as cancer, stroke, and Parkinson's disease.
Authors:
David W Koh; Ted M Dawson; Valina L Dawson
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Pharmacological research : the official journal of the Italian Pharmacological Society     Volume:  52     ISSN:  1043-6618     ISO Abbreviation:  Pharmacol. Res.     Publication Date:  2005 Jul 
Date Detail:
Created Date:  2005-05-24     Completed Date:  2005-08-25     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8907422     Medline TA:  Pharmacol Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  5-14     Citation Subset:  IM    
Affiliation:
Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 North Broadway St., Suite 711, Baltimore, MD 21205, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Apoptosis Inducing Factor
Brain Injuries / drug therapy
Enzyme Inhibitors / therapeutic use
Flavoproteins / physiology
Glycoside Hydrolases / physiology
Humans
Membrane Proteins / physiology
NF-kappa B / physiology
Necrosis
Neurons / pathology
Parkinson Disease / drug therapy
Poly(ADP-ribose) Polymerases / antagonists & inhibitors,  physiology*
Stroke / drug therapy
Chemical
Reg. No./Substance:
0/AIFM1 protein, human; 0/Apoptosis Inducing Factor; 0/Enzyme Inhibitors; 0/Flavoproteins; 0/Membrane Proteins; 0/NF-kappa B; EC 2.4.2.30/PARP1 protein, human; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.2.1.-/Glycoside Hydrolases; EC 3.2.1.143/poly ADP-ribose glycohydrolase

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


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