| pubmed-article:11146619 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11146619 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
| pubmed-article:11146619 | lifeskim:mentions | umls-concept:C0525037 | lld:lifeskim |
| pubmed-article:11146619 | lifeskim:mentions | umls-concept:C1155874 | lld:lifeskim |
| pubmed-article:11146619 | lifeskim:mentions | umls-concept:C0293304 | lld:lifeskim |
| pubmed-article:11146619 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:11146619 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:11146619 | lifeskim:mentions | umls-concept:C1516044 | lld:lifeskim |
| pubmed-article:11146619 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:11146619 | pubmed:dateCreated | 2001-1-26 | lld:pubmed |
| pubmed-article:11146619 | pubmed:abstractText | DAP kinase is a pro-apoptotic calcium-regulated serine/threonine kinase, whose expression is frequently lost in human tumours. Here we show that DAP kinase counteracts oncogene-induced transformation by activating a p19ARF/p53-dependent apoptotic checkpoint. Ectopic expression of DAP kinase suppressed oncogenic transformation of primary embryonic fibroblasts by activating p53 in a p19ARF-dependent manner. Consequently, the fibroblasts underwent apoptosis, characterized by caspase activation and DNA fragmentation. In response to c-Myc or E2F-1, the endogenous DAP kinase protein was upregulated. Furthermore, functional or genetic inactivation of the endogenous DAP kinase reduced the extent of induction of p19ARF/p53 and weakened the subsequent apoptotic responses to c-Myc or E2F-1. These results establish a role for DAP kinase in an early apoptotic checkpoint designed to eliminate pre-malignant cells during cancer development. | lld:pubmed |
| pubmed-article:11146619 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11146619 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11146619 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11146619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11146619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11146619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11146619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11146619 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11146619 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:11146619 | pubmed:issn | 1465-7392 | lld:pubmed |
| pubmed-article:11146619 | pubmed:author | pubmed-author:HorwitzM SMS | lld:pubmed |
| pubmed-article:11146619 | pubmed:author | pubmed-author:KinskyC BCB | lld:pubmed |
| pubmed-article:11146619 | pubmed:author | pubmed-author:DePinhoR ARA | lld:pubmed |
| pubmed-article:11146619 | pubmed:author | pubmed-author:RavelPP | lld:pubmed |
| pubmed-article:11146619 | pubmed:author | pubmed-author:DroguettGG | lld:pubmed |
| pubmed-article:11146619 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11146619 | pubmed:volume | 3 | lld:pubmed |
| pubmed-article:11146619 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11146619 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11146619 | pubmed:pagination | 1-7 | lld:pubmed |
| pubmed-article:11146619 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11146619 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11146619 | pubmed:articleTitle | DAP kinase activates a p19ARF/p53-mediated apoptotic checkpoint to suppress oncogenic transformation. | lld:pubmed |
| pubmed-article:11146619 | pubmed:affiliation | Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel. | lld:pubmed |
| pubmed-article:11146619 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11146619 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11146619 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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