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Blood, 1 January 2005, Vol. 105, No. 1, pp. 292-300.
Prepublished online as a Blood First Edition Paper on August 26, 2004; DOI 10.1182/blood-2004-03-1185.
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Submitted March 29, 2004
Accepted July 26, 2004
Physical and functional link of the leukemia-associated factors AML1 and PML
Lan Anh Nguyen, Pier Paolo Pandolfi, Yukiko Aikawa, Yusuke Tagata, Misao Ohki, and Issay Kitabayashi*
Molecular Oncology Division, National Cancer Center Research Institute, Tokyo, Japan
Molecular Biology Program and Department of Pathology, Sloan-Kettering Institute Memorial Sloan-Kettering Cancer Center, New York, NY, USA
Cancer Genomics Project, National Cancer Center Research Institute, Tokyo, Japan
* Corresponding author; email: ikitabay{at}gan2.ncc.go.jp.
The AML1-CBF transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML). The 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.
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