Linked Life Data

16015365

Source:http://linkedlifedata.com/resource/pubmed/id/16015365

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2005-7-14
pubmed:abstractText
Caspase activation has been frequently viewed as synonymous with apoptotic cell death; however, caspases can also contribute to processes that do not culminate in cell demise. Moreover, inhibition of caspases can have cytoprotective effects. In a number of different models, caspase inhibition does not maintain cellular viability and instead shifts the morphology of death from apoptosis to nonapoptotic pathways. Here, we explore the contribution of caspases to cell death, either as upstream signals or as downstream effectors contributing to apoptotic morphology, as well as alternative strategies for cell death inhibition. Such alternative strategies may either target catabolic hydrolases or be aimed at preventing mitochondrial membrane permeabilization and its upstream triggers.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1078-8956
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
725-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Caspase-independent cell death.
pubmed:affiliation
Centre National de la Recherche Scientifique, UMR8125, Institut Gustave Roussy, 39 rue Camille-Desmoulins, F-94805 Villejuif, France. kroemer@igr.fr
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't