Document Detail


Sphingomyelin breakdown and cell fate.
MedLine Citation:
PMID:  9009829     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A growing number of cell-surface receptors are now being shown to generate signals that trigger the hydrolysis of sphingomyelin to release diffusible ceramides. Ceramides have been implicated as key mediators in signaling pathways, with outcomes as diverse as cell proliferation, differentiation, growth arrest and apoptosis. The response depends on cell type, whether the signal is integrated with other signals originating from the same receptor and on the subcellular location of sphingomyelin hydrolysis and ceramide release.
Authors:
R Testi
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Trends in biochemical sciences     Volume:  21     ISSN:  0968-0004     ISO Abbreviation:  Trends Biochem. Sci.     Publication Date:  1996 Dec 
Date Detail:
Created Date:  1997-02-27     Completed Date:  1997-02-27     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7610674     Medline TA:  Trends Biochem Sci     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  468-71     Citation Subset:  IM    
Affiliation:
Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Italy. tesrob@flashnet.it
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD95 / metabolism
Cell Death / physiology*
Ceramides / metabolism*
Enzyme Activation
Forecasting
Humans
Hydrolysis
Models, Biological
Phosphoric Monoester Hydrolases / metabolism
Protein Kinases / metabolism
Receptors, Tumor Necrosis Factor / metabolism
Sphingomyelin Phosphodiesterase / metabolism
Sphingomyelins / metabolism,  physiology*
Chemical
Reg. No./Substance:
0/Antigens, CD95; 0/Ceramides; 0/Receptors, Tumor Necrosis Factor; 0/Sphingomyelins; EC 2.7.-/Protein Kinases; EC 3.1.3.-/Phosphoric Monoester Hydrolases; EC 3.1.4.12/Sphingomyelin Phosphodiesterase

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


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