| Literature DB >> 15331439 |
Lan Anh Nguyen1, Pier Paolo Pandolfi, Yukiko Aikawa, Yusuke Tagata, Misao Ohki, Issay Kitabayashi.
Abstract
The AML1-CBFbeta transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML). The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation. Here we report that a specific isoform PML I forms a complex with AML1. PML I was able to recruit AML1 and coactivator p300 in PML nuclear bodies and enhance the AML1-mediated transcription in the presence of p300. A specific C-terminal region of PML I and a C-terminal region of AML1 were found to be required for both their association and colocalization in the nuclear bodies. Overexpression of PML I stimulates myeloid cells to differentiate. These results suggest that PML I could act as a mediator for AML1 and its coactivator p300/CBP to assemble into functional complexes and, consequently, activate AML1-dependent transcription and myeloid cell differentiation.Entities:
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Year: 2004 PMID: 15331439 DOI: 10.1182/blood-2004-03-1185
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113