pubmed-article:11437412 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11437412 | lifeskim:mentions | umls-concept:C0600139 | lld:lifeskim |
pubmed-article:11437412 | lifeskim:mentions | umls-concept:C1326205 | lld:lifeskim |
pubmed-article:11437412 | lifeskim:mentions | umls-concept:C1518174 | lld:lifeskim |
pubmed-article:11437412 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
pubmed-article:11437412 | lifeskim:mentions | umls-concept:C0376515 | lld:lifeskim |
pubmed-article:11437412 | lifeskim:mentions | umls-concept:C1258295 | lld:lifeskim |
pubmed-article:11437412 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:11437412 | pubmed:dateCreated | 2001-7-4 | lld:pubmed |
pubmed-article:11437412 | pubmed:abstractText | Interactions between proteins of the Bcl-2 family play an important role in the regulation of apoptosis. Anti-apoptotic family members can heterodimerize with pro-apoptotic family members and antagonize their function, thus protecting against death. In cells protected from death by overexpression of Bcl-2 much of the Bax is present in Bax/Bcl-2 hetero-multimers and its death signal is blocked as it cannot homodimerize. This led us to use the Bcl-2/Bax heterodimer as a target for new compounds which may provide a therapy particularly suited to tumour cells for which resistance to conventional therapy is associated with elevated expression of Bcl-2. We assessed whether apoptosis could be induced in prostate tumour cells by blocking this heterodimerization with synthetic peptide sequences derived from the BH3 domain of pro-apoptotic Bcl-2 family members. Prostate cells were found to undergo up to 40% apoptosis 48 h following the introduction of synthetic peptides from the BH3 domains of Bax and Bak. The caspase inhibitor z-VAD.fmk provided protection against apoptosis mediated by these peptides. Immunoprecipitation studies revealed that introduction of peptides derived from the BH3 regions of Bak and Bax into cells blocked Bak/Bcl-2 heterodimerization. These data suggest that by blocking the dimerization through which Bcl-2 would normally inhibit apoptosis the apoptotic pathway driven by Bak was re-opened. | lld:pubmed |
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pubmed-article:11437412 | pubmed:language | eng | lld:pubmed |
pubmed-article:11437412 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11437412 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11437412 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11437412 | pubmed:month | Jul | lld:pubmed |
pubmed-article:11437412 | pubmed:issn | 0007-0920 | lld:pubmed |
pubmed-article:11437412 | pubmed:author | pubmed-author:MorganBB | lld:pubmed |
pubmed-article:11437412 | pubmed:author | pubmed-author:CotterT GTG | lld:pubmed |
pubmed-article:11437412 | pubmed:author | pubmed-author:PrevostGG | lld:pubmed |
pubmed-article:11437412 | pubmed:author | pubmed-author:CurtisJ MJM | lld:pubmed |
pubmed-article:11437412 | pubmed:author | pubmed-author:FinneganN MNM | lld:pubmed |
pubmed-article:11437412 | pubmed:copyrightInfo | Copyright 2001 Cancer Research Campaign. | lld:pubmed |
pubmed-article:11437412 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11437412 | pubmed:day | 6 | lld:pubmed |
pubmed-article:11437412 | pubmed:volume | 85 | lld:pubmed |
pubmed-article:11437412 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11437412 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11437412 | pubmed:pagination | 115-21 | lld:pubmed |
pubmed-article:11437412 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:11437412 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11437412 | pubmed:articleTitle | Induction of apoptosis in prostate carcinoma cells by BH3 peptides which inhibit Bak/Bcl-2 interactions. | lld:pubmed |
pubmed-article:11437412 | pubmed:affiliation | Dept of Biochemistry, University College Cork, Lee Maltings, Prospect Row, Cork, Ireland. | lld:pubmed |
pubmed-article:11437412 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11437412 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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