Linked Life Data

19150424

Source:http://linkedlifedata.com/resource/pubmed/id/19150424

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-1-19
pubmed:abstractText
Although mRNAs of multiple isoforms of Bax, which encodes a central regulator of apoptosis signaling, have been reported, only Baxalpha protein has been well documented and studied. Baxalpha exists in latent form and is activated upon apoptosis induction through conformational changes. Here we demonstrate that Baxbeta protein is ubiquitously present among human cells, but its activity is restricted through stringent regulation by proteasomal degradation. In contrast to Baxalpha, native Baxbeta spontaneously integrates into mitochondrial membrane and is highly potent in inducing cytochrome c release from mitochondria. Remarkably, Baxbeta protein is upregulated by apoptotic stimuli via inhibition of its ubiquitination process, and stable expression of Baxbeta in HCT116-Bax(-/-) cells restores their sensitivity to multiple stimuli. Baxbeta associates with and promotes Baxalpha activation. Moreover, selective knockdown of Baxbeta desensitizes HCT116-Bax(+/-) cells to Bax-dependent apoptosis signaling. These observations underscore the plasticity of human Bax in serving its role as a "gatekeeper" for apoptosis.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1097-4164
pubmed:author
pubmed:issnType
Electronic
pubmed:day
16
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
15-29
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Baxbeta: a constitutively active human Bax isoform that is under tight regulatory control by the proteasomal degradation mechanism.
pubmed:affiliation
Institute of Molecular and Cell Biology, Agency for Science, Technology, and Research, 61 Biopolis Drive, Singapore 138673, Republic of Singapore.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't