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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
24
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pubmed:dateCreated |
2007-6-13
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pubmed:abstractText |
The multidomain proapoptotic protein Bax of the Bcl-2 family is a central regulator for controlling the release of apoptogenic factors from mitochondria. Recent evidence suggests that the Bax-associating protein MOAP-1 may act as an effector for promoting Bax function in mitochondria. Here, we report that MOAP-1 protein is rapidly up-regulated by multiple apoptotic stimuli in mammalian cells. MOAP-1 is a short-lived protein (t(1/2) approximately 25 min) that is constitutively degraded by the ubiquitin-proteasome system. Induction of MOAP-1 by apoptotic stimuli ensues through inhibition of its polyubiquitination process. Elevation of MOAP-1 levels sensitizes cells to apoptotic stimuli and promotes recombinant Bax-mediated cytochrome c release from isolated mitochondria. Mitochondria depleted of short-lived proteins by cycloheximide (CHX) become resistant to Bax-mediated cytochrome c release. Remarkably, incubation of these mitochondria with in vitro-translated MOAP-1 effectively restores the cytochrome c releasing effect of recombinant Bax. We propose that apoptotic stimuli can facilitate the proapoptotic function of Bax in mitochondria through stabilization of MOAP-1.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-11060313,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-11163212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-11253367,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-11326099,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-11359904,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-11583631,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-11711427,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-11836513,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-12783855,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-14507994,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-14532004,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-14704432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-14744430,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-14744432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15008953,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15068805,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15122206,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15286356,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15719025,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15767553,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15803136,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15803138,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15837787,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15901672,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-15949439,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16094403,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16096654,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16199525,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16243507,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16344548,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16479014,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16551634,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16697956,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16816840,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-16892093,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-9020141,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17535899-9108035
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
12
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pubmed:volume |
104
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
10051-6
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:17535899-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:17535899-Apoptosis,
pubmed-meshheading:17535899-Apoptosis Regulatory Proteins,
pubmed-meshheading:17535899-Breast Neoplasms,
pubmed-meshheading:17535899-Cell Line, Tumor,
pubmed-meshheading:17535899-Female,
pubmed-meshheading:17535899-HCT116 Cells,
pubmed-meshheading:17535899-Half-Life,
pubmed-meshheading:17535899-Humans,
pubmed-meshheading:17535899-Mitochondria,
pubmed-meshheading:17535899-Proteasome Endopeptidase Complex,
pubmed-meshheading:17535899-Recombinant Proteins,
pubmed-meshheading:17535899-Ubiquitin,
pubmed-meshheading:17535899-bcl-2-Associated X Protein
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pubmed:year |
2007
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pubmed:articleTitle |
Inhibition of ubiquitin-mediated degradation of MOAP-1 by apoptotic stimuli promotes Bax function in mitochondria.
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pubmed:affiliation |
Institute of Molecular and Cell Biology, 61 Biopolis Drive (Proteos), Singapore 138673.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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