HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 283, Issue 16, 10476-10484, April 18, 2008

This Article Full Text Full Text (PDF) All Versions of this Article: 283/16/10476    most recent M709643200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted 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 Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kathrein, K. L. Articles by Winandy, S. Search for Related Content PubMed PubMed Citation Articles by Kathrein, K. L. Articles by Winandy, S. Social Bookmarking                      What's this?

Ikaros Directly Represses the Notch Target Gene Hes1 in a Leukemia T Cell Line

IMPLICATIONS FOR CD4 REGULATION^*

From the Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611

Ikaros and Notch1, two regulators of gene transcription, are critically important at many stages of T cell development. Deregulation of Ikaros and Notch activities cooperate to promote T cell leukemogenesis, providing evidence that they function in converging pathways in developing T cells. In this report, a mechanism for Ikaros:Notch cooperativity is described, revealing a non-redundant role for Ikaros in regulating expression of the Notch target gene Hes1 in a leukemia T cell line. We provide evidence that Ikaros directly represses Hes1 in concert with the transcriptional repressor, RBP-J, allowing for cross-talk between Notch and Ikaros that impacts regulation of CD4 expression. Taken together, these data describe a potential mechanism for Ikaros' function during T cell development and define Ikaros as an obligate repressor of Hes1.

Received for publication, November 27, 2007 , and in revised form, January 30, 2008.

^* This work was supported in part American Cancer Society Grant RSG-04-054-01-GMC and National Institutes of Health Grant R01 CA104962-01A1 (to S. W.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported by a Cellular and Molecular Basis of Disease Training Grant, funded by National Institutes of Health Grant T32 GM08061.

² To whom correspondence should be addressed: 320 E. Superior St., Morton 6-654, Chicago, IL 60611. Tel.: 312-503-3075; Fax: 312-503-1339; E-mail: s-winandy{at}northwestern.edu.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				J. A. Urban, W. Brugmann, and S. Winandy Cutting Edge: Ikaros Null Thymocytes Mature into the CD4 Lineage with Reduced TCR Signal: A Study Using CD3{zeta} Immunoreceptor Tyrosine-Based Activation Motif Transgenic Mice J. Immunol., April 1, 2009; 182(7): 3955 - 3959. [Abstract] [Full Text] [PDF]

				S. Chari and S. Winandy Ikaros Regulates Notch Target Gene Expression in Developing Thymocytes J. Immunol., November 1, 2008; 181(9): 6265 - 6274. [Abstract] [Full Text] [PDF]