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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-03-1185v1 105/1/292    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Nguyen, L. A. Articles by Kitabayashi, I. Search for Related Content PubMed PubMed Citation Articles by Nguyen, L. A. Articles by Kitabayashi, I. Related Collections Neoplasia Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA 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 From the Molecular Oncology Division, Cancer Genomics Project, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, Japan; and the Cancer Biology/Genetics Program and Department of Pathology, Sloan-Kettering Institute Memorial Sloan-Kethering Cancer Center, New York, NY The AML1-CBF 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. (Blood. 2005;105:292-300) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: B. Eun, Y. Lee, S. Hong, J. Kim, H.-W. Lee, K. Kim, W. Sun, and H. Kim Hes6 Controls Cell Proliferation via Interaction with cAMP-response Element-binding Protein-binding Protein in the Promyelocytic Leukemia Nuclear Body J. Biol. Chem., February 29, 2008; 283(9): 5939 - 5949. [Abstract] [Full Text] [PDF] H. Yoshida, H. Ichikawa, Y. Tagata, T. Katsumoto, K. Ohnishi, Y. Akao, T. Naoe, P. P. Pandolfi, and I. Kitabayashi PML-Retinoic Acid Receptor {alpha} Inhibits PML IV Enhancement of PU.1-Induced C/EBP{varepsilon} Expression in Myeloid Differentiation Mol. Cell. Biol., August 15, 2007; 27(16): 5819 - 5834. [Abstract] [Full Text] [PDF] N. Dror, N. Rave-Harel, A. Burchert, A. Azriel, T. Tamura, P. Tailor, A. Neubauer, K. Ozato, and B.-Z. Levi Interferon Regulatory Factor-8 Is Indispensable for the Expression of Promyelocytic Leukemia and the Formation of Nuclear Bodies in Myeloid Cells J. Biol. Chem., February 23, 2007; 282(8): 5633 - 5640. [Abstract] [Full Text] [PDF]

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