Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2007-4-4
pubmed:abstractText
Anoxia, the condition of oxygen deprivation, induces apoptosis via the intrinsic apoptotic pathway. Cells deficient in both Bax and Bak do not undergo cell death during anoxia. However, the underlying mechanism of anoxia induced cell death is not well defined. Here we report our latest findings of two critical events that are required to induce cell death during anoxia. First, a key member of the Bcl-2 family of pro-survival proteins, Mcl-1, undergoes proteasomal-dependent degradation. The loss of Mcl-1 protein is independent of Bax or Bak indicating this is an early event in the apoptotic cascade. Second, cells inhibit the mitochondrial electron transport chain to negate the pro-survival function of Bcl-2/Bcl-X(L). These observations indicate that loss of pro-survival function is necessary for anoxia induced cell death.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
807-9
pubmed:dateRevised
2008-7-9
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Role of Bcl-2 family members in anoxia induced cell death.
pubmed:affiliation
Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural