Linked Life Data

21122071

Source:http://linkedlifedata.com/resource/pubmed/id/21122071

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-12-16
pubmed:abstractText
Caspase-independent neuronal death has been shown to occur in neuroexcitotoxicity. Here, we tested the hypothesis that the gene encoding Bcl-2/E1B-19K-interacting protein 3 (BNIP3) mediates caspase-independent neuronal death in excitotoxicity. BNIP3 was not detectable in neurons under normal condition. BNIP3 expression was increased dramatically in neurons in both in vivo and in vitro models of excitotoxicity. Expression of full-length BNIP3 in primary hippocampal neurons induced atypical cell death that required protein synthesis but was largely independent of caspase activities. Inhibition of BNIP3 expression by RNA interference protected against glutamate-induced neuronal cell death. Thus, BNIP3 activation and expression appears to be both necessary and sufficient for neuronal apoptosis in excitotoxicity. These results suggest that BNIP3 may be a new target for neuronal rescue strategies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1742-4658
pubmed:author
pubmed:copyrightInfo
© 2010 The Authors Journal compilation © 2010 FEBS.
pubmed:issnType
Electronic
pubmed:volume
278
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
134-42
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
The proapoptotic member of the Bcl-2 family Bcl-2?/?E1B-19K-interacting protein 3 is a mediator of caspase-independent neuronal death in excitotoxicity.
pubmed:affiliation
Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Manitoba, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't