| pubmed-article:9531570 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9531570 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
| pubmed-article:9531570 | lifeskim:mentions | umls-concept:C1384567 | lld:lifeskim |
| pubmed-article:9531570 | lifeskim:mentions | umls-concept:C0023487 | lld:lifeskim |
| pubmed-article:9531570 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:9531570 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
| pubmed-article:9531570 | lifeskim:mentions | umls-concept:C1167622 | lld:lifeskim |
| pubmed-article:9531570 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:9531570 | lifeskim:mentions | umls-concept:C0765587 | lld:lifeskim |
| pubmed-article:9531570 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:9531570 | pubmed:dateCreated | 1998-5-12 | lld:pubmed |
| pubmed-article:9531570 | pubmed:abstractText | Typical acute promyelocytic leukemia (APL) is associated with expression of the PML-RARalpha fusion protein and responsiveness to treatment with all-trans retinoic acid (ATRA). A rare, but recurrent, APL has been described that does not respond to ATRA treatment and is associated with a variant chromosomal translocation and expression of the PLZF-RARalpha fusion protein. Both PML- and PLZF-RARalpha possess identical RAR sequences and inhibit ATRA-induced gene transcription as well as cell differentiation. We now show that the above-mentioned oncogenic fusion proteins interact with the nuclear receptor corepressor N-CoR and, in comparison with the wild-type RARalpha protein, their interactions display reduced sensitivities to ATRA. Although pharmacologic concentration of ATRA could still induce dissociation of N-CoR from PML-RARalpha, it had a very little effect on its association with the PLZF-RARalpha fusion protein. This ATRA-insensitive interaction between N-CoR and PLZF-RARalpha was mediated by the N-terminal PLZF moiety of the chimera. It appears that N-CoR/histone deacetylase corepressor complex interacts directly in an ATRA-insensitive manner with the BTB/POZ-domain of the wild-type PLZF protein and is required, at least in part, for its function as a transcriptional repressor. As the above-noted results predict, histone deacetylase inhibitors antagonize oncogenic activities of the PML-RARalpha fusion protein and partially relieve transcriptional repression by PLZF as well as inhibitory effect of PLZF-RARalpha on ATRA response. Taken together, our results demonstrate involvement of nuclear receptor corepressor/histone deacetylase complex in the molecular pathogenesis of APL and provide an explanation for differential sensitivities of PML- and PLZF-RARalpha-associated leukemias to ATRA. | lld:pubmed |
| pubmed-article:9531570 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9531570 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9531570 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9531570 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:9531570 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9531570 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:9531570 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:9531570 | pubmed:author | pubmed-author:WaxmanSS | lld:pubmed |
| pubmed-article:9531570 | pubmed:author | pubmed-author:ZinRR | lld:pubmed |
| pubmed-article:9531570 | pubmed:author | pubmed-author:SöderströmMM | lld:pubmed |
| pubmed-article:9531570 | pubmed:author | pubmed-author:ZelentAA | lld:pubmed |
| pubmed-article:9531570 | pubmed:author | pubmed-author:GuidezFF | lld:pubmed |
| pubmed-article:9531570 | pubmed:author | pubmed-author:IvinsSS | lld:pubmed |
| pubmed-article:9531570 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9531570 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:9531570 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:9531570 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9531570 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9531570 | pubmed:pagination | 2634-42 | lld:pubmed |
| pubmed-article:9531570 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:9531570 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9531570 | pubmed:articleTitle | Reduced retinoic acid-sensitivities of nuclear receptor corepressor binding to PML- and PLZF-RARalpha underlie molecular pathogenesis and treatment of acute promyelocytic leukemia. | lld:pubmed |
| pubmed-article:9531570 | pubmed:affiliation | Leukaemia Research Fund Centre at the Institute of Cancer Research, Chester Beatty Laboratories, London, UK. | lld:pubmed |
| pubmed-article:9531570 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9531570 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9531570 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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