Linked Life Data

12652643

Source:http://linkedlifedata.com/resource/pubmed/id/12652643

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-3-24
pubmed:abstractText
An increase in the permeability of the outer mitochondrial membrane is central to apoptotic cell death, since it leads to the release of several apoptogenic factors, such as cytochrome c and Smac/Diablo, into the cytoplasm that activate downstream death programs. During apoptosis, the mitochondria also release AIF and endonuclease G, both of which are translocated to the nucleus and are implicated in apoptotic nuclear changes that occur in a caspase-independent manner. Mitochondrial membrane permeability is directly controlled by the major apoptosis regulator, i.e., the Bcl-2 family of proteins, mainly through regulation of the formation of apoptotic protein-conducting pores in the outer mitochondrial membrane, although the precise molecular mechanisms are still not completely understood. Here, I focus on the mechanisms by which Bcl-2 family members control the permeability of mitochondrial membrane during apoptosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-9541
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
195
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
158-67
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Cell death regulation by the Bcl-2 protein family in the mitochondria.
pubmed:affiliation
Osaka University Graduate School of Medicine, Department of Post-Genomics and Diseases, Laboratory of Molecular Genetics, CREST of Japanese Science and Technology, Suita, Osaka, Japan. tsujimot@gene.med.osaka-u.ac.jp
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't