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Related Collections Neoplasia Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 May 2001, Vol. 97, No. 9, pp. 2815-2822 NEOPLASIA The corepressor CtBP interacts with Evi-1 to repress transforming growth factor  signaling Koji Izutsu, Mineo Kurokawa, Yoichi Imai, Kazuhiro Maki, Kinuko Mitani, and Hisamaru Hirai From the Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Japan. Evi-1 is a zinc finger nuclear protein whose inappropriate expression leads to leukemic transformation of hematopoietic cells in mice and humans. This was previously shown to block the antiproliferative effect of transforming growth factor  (TGF-). Evi-1 represses TGF- signaling by direct interaction with Smad3 through its first zinc finger motif. Here, it is demonstrated that Evi-1 represses Smad-induced transcription by recruiting C-terminal binding protein (CtBP) as a corepressor. Evi-1 associates with CtBP1 through one of the consensus binding motifs, and this association is required for efficient inhibition of TGF- signaling. A specific inhibitor for histone deacetylase (HDAc) alleviates Evi-1-mediated repression of TGF- signaling, suggesting that HDAc is involved in the transcriptional repression by Evi-1. This identifies a novel function of Evi-1 as a member of corepressor complexes and suggests that aberrant recruitment of corepressors is one of the mechanisms for Evi-1-induced leukemogenesis. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Alpatov, Y. Shi, G. C. Munguba, B. Moghimi, J.-H. Joo, J. Bungert, and S. P. Sugrue Corepressor CtBP and Nuclear Speckle Protein Pnn/DRS Differentially Modulate Transcription and Splicing of the E-Cadherin Gene Mol. Cell. Biol., March 1, 2008; 28(5): 1584 - 1595. 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