| pubmed-article:17178918 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17178918 | lifeskim:mentions | umls-concept:C1070653 | lld:lifeskim |
| pubmed-article:17178918 | lifeskim:mentions | umls-concept:C0024264 | lld:lifeskim |
| pubmed-article:17178918 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:17178918 | lifeskim:mentions | umls-concept:C1326205 | lld:lifeskim |
| pubmed-article:17178918 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:17178918 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:17178918 | lifeskim:mentions | umls-concept:C0445450 | lld:lifeskim |
| pubmed-article:17178918 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:17178918 | pubmed:dateCreated | 2006-12-27 | lld:pubmed |
| pubmed-article:17178918 | pubmed:abstractText | The physiological role of B cell lymphoma 2 (Bcl-2) homology 3-only proteins has been investigated in mice lacking the individual genes identifying rate-limiting roles for Bim (Bcl-2-interacting mediator of cell death) and Puma (p53-up-regulated modulator of apoptosis) in apoptosis induction. The loss of Bim protects lymphocytes from apoptosis induced by cytokine deprivation and deregulated Ca++ flux and interferes with the deletion of autoreactive lymphocytes and the shutdown of immune responses. In contrast, Puma is considered the key mediator of p53-induced apoptosis. To investigate the hypothesis that Bim and Puma have overlapping functions, we generated mice lacking both genes and found that bim-/-/puma-/- animals develop multiple postnatal defects that are not observed in the single knockout mice. Most strikingly, hyperplasia of lymphatic organs is comparable with that observed in mice overexpressing Bcl-2 in all hemopoietic cells exceeding the hyperplasia observed in bim-/- mice. Bim and Puma also have clearly overlapping functions in p53-dependent and -independent apoptosis. Their combined loss promotes spontaneous tumorigenesis, causing the malignancies observed in Bcl-2 transgenic mice, but does not exacerbate the autoimmunity observed in the absence of Bim. | lld:pubmed |
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| pubmed-article:17178918 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17178918 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17178918 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17178918 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17178918 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:17178918 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:HäckerGeorgG | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:ManzlClaudiaC | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:StrasserAndre... | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:MichalakEwaE | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:BöckGüntherG | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:TzankovAlexan... | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:VillungerAndr... | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:ErlacherMiria... | lld:pubmed |
| pubmed-article:17178918 | pubmed:author | pubmed-author:LabiVerenaV | lld:pubmed |
| pubmed-article:17178918 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17178918 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:17178918 | pubmed:volume | 203 | lld:pubmed |
| pubmed-article:17178918 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17178918 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17178918 | pubmed:pagination | 2939-51 | lld:pubmed |
| pubmed-article:17178918 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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