Ikaros directly represses the notch target gene Hes1 in a leukemia T cell line: implications for CD4 regulation.
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-Jkappa, 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.[1]References
- Ikaros directly represses the notch target gene Hes1 in a leukemia T cell line: implications for CD4 regulation. Kathrein, K.L., Chari, S., Winandy, S. J. Biol. Chem. (2008) [Pubmed]
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