Document Detail

The molecular mechanisms of neuronal apoptosis.
MedLine Citation:
PMID:  7849526     Owner:  NLM     Status:  MEDLINE    
During the past year, apoptosis has been recognized as a process that is perpetually poised to be initiated--often from the cytoplasm rather than from the nucleus--unless it is suppressed by survival factors. Suspected mediators of apoptosis that have recently been investigated include the cysteine protease interleukin-1 beta-converting enzyme, free radicals and cell cycle kinases. Known inhibitors of programmed cell death, such as Bcl-2 and its homologues, have been further studied, and the results suggest that cell death may be regulated by multiple pathways. With the recent identification of the Drosophila gene reaper, which appears to play a role in the initiation of apoptosis, another genetic system for studying cell death has become available.
L L Rubin; C L Gatchalian; G Rimon; S F Brooks
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Current opinion in neurobiology     Volume:  4     ISSN:  0959-4388     ISO Abbreviation:  Curr. Opin. Neurobiol.     Publication Date:  1994 Oct 
Date Detail:
Created Date:  1995-03-14     Completed Date:  1995-03-14     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9111376     Medline TA:  Curr Opin Neurobiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  696-702     Citation Subset:  IM    
Eisai London Laboratories, University College London, UK.
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MeSH Terms
Caspase 1
Cell Cycle
Cell Death
Cysteine Endopeptidases / physiology
Drosophila / genetics
Nerve Degeneration
Nervous System Diseases / pathology
Neurons / physiology*
Proto-Oncogene Proteins / physiology
Proto-Oncogene Proteins c-bcl-2
Reg. No./Substance:
0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; EC 3.4.22.-/Cysteine Endopeptidases; EC 1

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

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