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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6617
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pubmed:dateCreated |
1997-3-3
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pubmed:abstractText |
The protein p53 is a key tumour-suppressor, as evidenced by its frequent inactivation in human cancers. Animal models have indicated that attenuation of p53-dependent cell death (apoptosis) can contribute to both the initiation and progression of cancer, but the molecular mechanisms are unknown. Although p53-mediated transcriptional activation is one possible explanation, none of the known p53-responsive genes has been shown to function in p53-dependent apoptosis. Here we test the role of the death-promoting gene bax in a transgenic mouse brain tumour, a model in which p53-mediated apoptosis attenuates tumour growth. Inactivation of p53 causes a dramatic acceleration of tumour growth owing to a reduction in apoptosis of over ninety per cent. We show that p53-dependent expression of bax is induced in slow-growing apoptotic tumours. Moreover, tumour growth is accelerated and apoptosis drops by fifty per cent in Bax-deficient mice, indicating that it is required for a full p53-mediated response. To our knowledge this is the first demonstration that Bax acts as a tumour suppressor, and our findings indicate that Bax could be a component of the p53-mediated apoptotic response in this system.
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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/Bax protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0028-0836
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
13
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pubmed:volume |
385
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
637-40
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:9024662-Animals,
pubmed-meshheading:9024662-Apoptosis,
pubmed-meshheading:9024662-Brain Neoplasms,
pubmed-meshheading:9024662-Choroid Plexus,
pubmed-meshheading:9024662-Female,
pubmed-meshheading:9024662-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:9024662-Genes, Tumor Suppressor,
pubmed-meshheading:9024662-Male,
pubmed-meshheading:9024662-Mice,
pubmed-meshheading:9024662-Mice, Inbred C3H,
pubmed-meshheading:9024662-Mice, Transgenic,
pubmed-meshheading:9024662-Proto-Oncogene Proteins,
pubmed-meshheading:9024662-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:9024662-Tumor Suppressor Protein p53,
pubmed-meshheading:9024662-bcl-2-Associated X Protein
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pubmed:year |
1997
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pubmed:articleTitle |
Bax suppresses tumorigenesis and stimulates apoptosis in vivo.
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pubmed:affiliation |
Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine at Chapel Hill, 27599, USA.
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pubmed:publicationType |
Journal Article
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