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Selective potentiation of Stat-dependent gene expression by collaborator of Stat6 (CoaSt6), a transcriptional cofactor
Shreevrat Goenka*, and
*Department of Microbiology and Immunology and Division of Rheumatology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-2363
Edited by Philippa Marrack, National Jewish Medical and Research Center, Denver, CO, and approved January 17, 2006
Received for publication August 11, 2005.
The molecular mechanisms by which transcription is selectivelyactivated and precisely controlled by signal transducer andactivator of transcription (Stat) factors represent a centralissue in cytokine-mediated cellular responses. Stat6 mediatesresponses to IL-4 and antagonizes Stat1 activated by IFN-. Wehave discovered that Stat6 binds to collaborator of Stat6 (CoaSt6),a protein that lacks conventional coactivator motifs but containsthree iterations of a domain found in the variant histone macroH2A.Although macroH2A participates in transcriptional silencing,the macro domains of CoaSt6 increased IL-4-induced gene expression.Moreover, CoaSt6 amplified Stat6-mediated but not IFN--inducedgene expression, providing evidence of a selective coregulatorof Stat-mediated gene transcription.