Source:http://linkedlifedata.com/resource/pubmed/id/15198484
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2004-6-16
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pubmed:abstractText |
Bag-1 is a novel multifunctional protein. It was identified based on its ability to bind the anti-apoptotic protein, bcl-2, and also reported to interact with the heat shock protein 70 kDa (Hsp70). Thus, bag-1 may modulate apoptosis and the chaperone activity. More interestingly, bag-1 can bind to several growth factor receptors or steroid hormone receptors and regulate their function and signaling. The receptor of hepatocyte growth factor (HGF), c-met, associated with bag-1 in a study measuring immunoprecipitation in endothelial cells, we decided to investigate the contribution of bag-1 to the anti-apoptotic action of HGF. Endogenous expression of bag-1 in endothelial cells was confirmed mainly in the cytosol fraction. The treatment of human recombinant HGF (rHGF) increased tyrosine kinase and ERK phosphorylation, whereas over-expression of bag-1 had no effect on this phosphorylation. In DNA synthesis as assessed by thymidine incorporation, over-expression of bag-1 also did not induce any additional increase. In contrast, in an assay of cell death as assessed by caspase activity and lactate dehydrogenase release, over-expression of bag-1 alone attenuated serum-free and tumor necrosis factor-alpha-induced cell death in endothelial cells. No synergistic effect was observed between bag-1 and rHGF. To further study the association of HGF and bag-1, we examined the effect of a deletion mutant of the bag-1 C-terminal region (CTR), because bag-1 CTR is necessary to bind to c-met. Unexpectedly, over-expression of bag-1 CTR also attenuated the endothelial cell death, similar to rHGF. Taken together, these results indicate that over-expression of bag-1 has an anti-apoptotic effect on endothelial cells independent of HGF signaling.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/BCL2-associated athanogene 1 protein,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Hepatocyte Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-met,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0916-9636
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
359-65
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15198484-Animals,
pubmed-meshheading:15198484-Aorta,
pubmed-meshheading:15198484-Apoptosis,
pubmed-meshheading:15198484-Carrier Proteins,
pubmed-meshheading:15198484-Cattle,
pubmed-meshheading:15198484-Cell Division,
pubmed-meshheading:15198484-Cells, Cultured,
pubmed-meshheading:15198484-DNA-Binding Proteins,
pubmed-meshheading:15198484-Drug Synergism,
pubmed-meshheading:15198484-Endothelium, Vascular,
pubmed-meshheading:15198484-Gene Deletion,
pubmed-meshheading:15198484-Hepatocyte Growth Factor,
pubmed-meshheading:15198484-Humans,
pubmed-meshheading:15198484-Mitogen-Activated Protein Kinases,
pubmed-meshheading:15198484-Mutation,
pubmed-meshheading:15198484-Phosphorylation,
pubmed-meshheading:15198484-Protein-Tyrosine Kinases,
pubmed-meshheading:15198484-Proto-Oncogene Proteins c-met,
pubmed-meshheading:15198484-Recombinant Proteins,
pubmed-meshheading:15198484-Transcription Factors
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pubmed:year |
2004
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pubmed:articleTitle |
Lack of association between the hepatocyte growth factor receptor, c-met, and the anti-apoptotic action of bag-1 in endothelial cells.
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pubmed:affiliation |
Department of Geriatric Medicine, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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