pubmed-article:17227826 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17227826 | lifeskim:mentions | umls-concept:C0026764 | lld:lifeskim |
pubmed-article:17227826 | lifeskim:mentions | umls-concept:C1367453 | lld:lifeskim |
pubmed-article:17227826 | lifeskim:mentions | umls-concept:C0032112 | lld:lifeskim |
pubmed-article:17227826 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
pubmed-article:17227826 | lifeskim:mentions | umls-concept:C1171362 | lld:lifeskim |
pubmed-article:17227826 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
pubmed-article:17227826 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:17227826 | lifeskim:mentions | umls-concept:C1515670 | lld:lifeskim |
pubmed-article:17227826 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:17227826 | pubmed:dateCreated | 2007-4-23 | lld:pubmed |
pubmed-article:17227826 | pubmed:abstractText | Defects in apoptosis mechanisms play important roles in malignancy and autoimmunity. Orphan nuclear receptor Nur77/TR3 has been demonstrated to bind antiapoptotic protein Bcl-2 and convert it from a cytoprotective to a cytodestructive protein, representing a phenotypic conversion mechanism. Of the 6 antiapoptotic human Bcl-2 family members, we found that Nur77/TR3 binds strongest to Bcl-B, showing selective reactivity with Bcl-B, Bcl-2, and Bfl-1 but not Bcl-X(L), Mcl-1, or Bcl-W. Nur77 converts the phenotype of Bcl-B from antiapoptotic to proapoptotic. Bcl-B is prominently expressed in plasma cells and multiple myeloma. Endogenous Bcl-B associates with endogenous Nur77 in RPMI 8226 myeloma cells, where RNA interference experiments demonstrated dependence on Bcl-B for Nur77-induced apoptosis. Furthermore, a Nur77-mimicking peptide killed RPMI 8226 myeloma cells through a Bcl-B-dependent mechanism. Because Bcl-B is abundantly expressed in plasma cells and some myelomas, these findings raise the possibility of exploiting the Nur77/Bcl-B mechanism for apoptosis for eradication of autoimmune plasma cells or myeloma. | lld:pubmed |
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pubmed-article:17227826 | pubmed:language | eng | lld:pubmed |
pubmed-article:17227826 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17227826 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:17227826 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17227826 | pubmed:month | May | lld:pubmed |
pubmed-article:17227826 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:ReedJohn CJC | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:LichtensteinA... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:KrajewskaMary... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:KolluriSiva... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:SatterthwaitA... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:KrajewskiStan... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:ZhangXiao-Kun... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:FaustinBenjam... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:BrueyJean-Mar... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:LucianoFreder... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:ZhaiDayongD | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:Bailly-Maitre... | lld:pubmed |
pubmed-article:17227826 | pubmed:author | pubmed-author:Ortiz-RubioPa... | lld:pubmed |
pubmed-article:17227826 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17227826 | pubmed:day | 1 | lld:pubmed |
pubmed-article:17227826 | pubmed:volume | 109 | lld:pubmed |
pubmed-article:17227826 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17227826 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17227826 | pubmed:pagination | 3849-55 | lld:pubmed |
pubmed-article:17227826 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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