| pubmed-article:12509458 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C1267092 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C0027096 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C0021943 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C2717951 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C0162768 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C1514562 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C1883221 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C1883204 | lld:lifeskim |
| pubmed-article:12509458 | lifeskim:mentions | umls-concept:C1880389 | lld:lifeskim |
| pubmed-article:12509458 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12509458 | pubmed:dateCreated | 2003-1-1 | lld:pubmed |
| pubmed-article:12509458 | pubmed:abstractText | Inversion(16) is one of the most frequent chromosomal translocations found in acute myeloid leukemia (AML), occurring in over 8% of AML cases. This translocation results in a protein product that fuses the first 165 amino acids of core binding factor beta to the coiled-coil region of a smooth muscle myosin heavy chain (CBFbeta/SMMHC). CBFbeta interacts with AML1 to form a heterodimer that binds DNA; this interaction increases the affinity of AML1 for DNA. The CBFbeta/SMMHC fusion protein cooperates with AML1 to repress the transcription of AML1-regulated genes. We show that CBFbeta/SMMHC contains a repression domain in the C-terminal 163 amino acids of the SMMHC region that is required for inv(16)-mediated transcriptional repression. This minimal repression domain is sufficient for the association of CBFbeta/SMMHC with the mSin3A corepressor. In addition, the inv(16) fusion protein specifically associates with histone deacetylase 8 (HDAC8). inv(16)-mediated repression is sensitive to HDAC inhibitors. We propose a model whereby the inv(16) fusion protein associates with AML1 to convert AML1 into a constitutive transcriptional repressor. | lld:pubmed |
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| pubmed-article:12509458 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12509458 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12509458 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12509458 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12509458 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:12509458 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:12509458 | pubmed:author | pubmed-author:FriedmanAlan... | lld:pubmed |
| pubmed-article:12509458 | pubmed:author | pubmed-author:HiebertScott... | lld:pubmed |
| pubmed-article:12509458 | pubmed:author | pubmed-author:KummalueTanaw... | lld:pubmed |
| pubmed-article:12509458 | pubmed:author | pubmed-author:LutterbachBar... | lld:pubmed |
| pubmed-article:12509458 | pubmed:author | pubmed-author:DurstKristie... | lld:pubmed |
| pubmed-article:12509458 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12509458 | pubmed:volume | 23 | lld:pubmed |
