pubmed-article:9024662 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9024662 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:9024662 | lifeskim:mentions | umls-concept:C1326912 | lld:lifeskim |
pubmed-article:9024662 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:9024662 | pubmed:issue | 6617 | lld:pubmed |
pubmed-article:9024662 | pubmed:dateCreated | 1997-3-3 | lld:pubmed |
pubmed-article:9024662 | 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. | lld:pubmed |
pubmed-article:9024662 | pubmed:language | eng | lld:pubmed |
pubmed-article:9024662 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9024662 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9024662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9024662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9024662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9024662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9024662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9024662 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9024662 | pubmed:month | Feb | lld:pubmed |
pubmed-article:9024662 | pubmed:issn | 0028-0836 | lld:pubmed |
pubmed-article:9024662 | pubmed:author | pubmed-author:KorsmeyerS... | lld:pubmed |
pubmed-article:9024662 | pubmed:author | pubmed-author:KnudsonC MCM | lld:pubmed |
pubmed-article:9024662 | pubmed:author | pubmed-author:Van DykeTT | lld:pubmed |
pubmed-article:9024662 | pubmed:author | pubmed-author:HuY WYW | lld:pubmed |
pubmed-article:9024662 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9024662 | pubmed:day | 13 | lld:pubmed |
pubmed-article:9024662 | pubmed:volume | 385 | lld:pubmed |
pubmed-article:9024662 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9024662 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9024662 | pubmed:pagination | 637-40 | lld:pubmed |
pubmed-article:9024662 | pubmed:dateRevised | 2005-11-17 | lld:pubmed |
pubmed-article:9024662 | pubmed:meshHeading | pubmed-meshheading:9024662-... | lld:pubmed |
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pubmed-article:9024662 | pubmed:meshHeading | pubmed-meshheading:9024662-... | lld:pubmed |
pubmed-article:9024662 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9024662 | pubmed:articleTitle | Bax suppresses tumorigenesis and stimulates apoptosis in vivo. | lld:pubmed |
pubmed-article:9024662 | pubmed:affiliation | Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine at Chapel Hill, 27599, USA. | lld:pubmed |
pubmed-article:9024662 | pubmed:publicationType | Journal Article | lld:pubmed |
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