Linked Life Data

17584989

Source:http://linkedlifedata.com/resource/pubmed/id/17584989

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2007-12-17
pubmed:abstractText
Bim is a proapoptotic BH3-domain-only member of the Bcl-2 family, and its expression is regulated both transcriptionally and posttranslationally. We developed an in vitro system examining the posttranslational regulation of Bim. Since Bim is a strong mediator of apoptosis, it has been quite difficult to establish cell lines stably overexpressing Bim. Coexpression of Bcl-2 enabled us to obtain mouse embryonic fibroblasts (MEFs) in which Bim is overexpressed and Bcl-2 expression is regulated by Tet-off system. Reduction of Bcl-2 levels by doxycycline treatment induced caspase-3 and caspase-7 activation, which was followed by Bim degradation. Bim degradation was suppressed by gene knockdown of caspase-3, but not by caspase-7 knockdown. The same posttranslational regulation of Bim was observed in osteoclasts. These results suggest that caspase-3 negatively regulates Bim expression by stimulating its degradation, thus creating a negative feedback loop in the Bim-caspase axis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
1116
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
271-80
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Posttranslational regulation of Bim by caspase-3.
pubmed:affiliation
Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't