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Protein kinase C0 modulates nuclear receptor-corepressor interaction during T cell activation

  1. Author:
    Ishaq, M.
    DeGray, G.
    Natarajan, V.

  2. Author Address

    NCI, Mol Cell Biol Lab, Sci Applicat Int Corp, Frederick, MD 21702 USA NCI, Mol Cell Biol Lab, Sci Applicat Int Corp, Frederick, MD 21702 USA Ishaq M NCI, Mol Cell Biol Lab, Sci Applicat Int Corp, Frederick, MD 21702 USA
    1. Year: 2003
  2. Journal: Journal of Biological Chemistry
    1. 278
    2. 41
    3. Pages: 39296-39302
  4. Type of Article: Article
  1. Abstract:

    Transcriptional repression by nuclear receptor corepressors plays a critical role in T cell development. However, the role of these corepressors in T cell activation is poorly understood. We report that T cell activation silenced transcription driven by nuclear receptors retinoic acid receptor, retinoid X receptor, and thyroid hormone receptor and induced silencing mediator of retinoic acid and thyroid hormone receptors (SMRT)-receptor interaction. Whereas the expression of a dominant active mutant of protein kinase Ctheta (PKCtheta) induced strong SMRT-receptor interaction in the absence of T cell activation, a dominant negative mutant of PKCtheta decreased the interaction. Loss of PKCtheta expression by induction of "RNA interference" resulted in the attenuation of basal and activation-induced SMRT-receptor interaction. We suggest that T cell activation silences nuclear receptor- dependent transactivation in part through PKCtheta-dependent enhancement of SMRT-receptor interaction.

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