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An acute myeloid leukemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms.

1995; Springer Nature; Volume: 14; Issue: 2 Linguagem: Inglês

10.1002/j.1460-2075.1995.tb07008.x

1460-2075

Tomoyuki Tanaka, Kozo Tanaka, Seishi Ogawa, Mineo Kurokawa, Kinuko Mitani, Junji Nishida, Yoshihiro Shibata, Y Yazaki, Hisamaru Hirai,

Epigenetics and DNA Methylation

Research Article16 January 1995free access An acute myeloid leukemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms. T. Tanaka T. Tanaka Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author K. Tanaka K. Tanaka Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author S. Ogawa S. Ogawa Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author M. Kurokawa M. Kurokawa Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author K. Mitani K. Mitani Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author J. Nishida J. Nishida Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author Y. Shibata Y. Shibata Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author Y. Yazaki Y. Yazaki Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author H. Hirai H. Hirai Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author T. Tanaka T. Tanaka Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author K. Tanaka K. Tanaka Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author S. Ogawa S. Ogawa Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author M. Kurokawa M. Kurokawa Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author K. Mitani K. Mitani Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author J. Nishida J. Nishida Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author Y. Shibata Y. Shibata Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author Y. Yazaki Y. Yazaki Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author H. Hirai H. Hirai Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. Search for more papers by this author Author Information T. Tanaka1, K. Tanaka1, S. Ogawa1, M. Kurokawa1, K. Mitani1, J. Nishida1, Y. Shibata1, Y. Yazaki1 and H. Hirai1 1Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. The EMBO Journal (1995)14:341-350https://doi.org/10.1002/j.1460-2075.1995.tb07008.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info The AML1 gene on chromosome 21 is disrupted in the (8;21)(q22;q22) and (3;21)(q26;q22) translocations associated with myelogenous leukemias and encodes a DNA binding protein. From the AML1 gene, two representative forms of proteins, AML1a and AML1b, are produced by alternative splicing. Both forms have a DNA binding domain but, unlike AML1b, AML1a lacks a putative transcriptional activation domain. Here we demonstrate that overexpressed AML1a totally suppresses granulocytic differentiation and stimulates cell proliferation in 32Dcl3 murine myeloid cells treated with granulocyte colony-stimulating factor. These effects of AML1a were canceled by the concomitant overexpression of AML1b. Such biological phenomena could be explained by our observations that (i) AML1a, which on its own has no effects as a transcriptional regulator, dominantly suppresses transcriptional activation by AML1b, and (ii) AML1a exhibits the higher affinity for DNA binding compared with AML1b. These antagonistic actions could be important in leukemogenesis and/or myeloid cell differentiation because more than half of myelogenous leukemia patients showed an increase in the relative amounts of AML1a. Previous ArticleNext Article Volume 14Issue 21 January 1995In this issue RelatedDetailsLoading ...