Tyrosine phosphorylation of PICOT and its translocation to the nucleus in response of human T cells to oxidative stress
Protein kinase C θ (PKCθ) is a Ca2+-independent isoform expressed in T but not B lymphocytes, and is therefore suggested as being linked to the T cell antigen receptor (TCR) function (1 2). PKCθ was shown to function as an upstream regulator of critical transcription factors, such as AP-1 and NF-KB, in activated T lymphocytes (3). More recent studies demonstrated that PKCθ colocalizes with the TCR at the core of the supramolecular activation complex (SMAC) formed at the contact region between antigen-responding T cells and antigen-presenting cells (APC) (4). Finally, PKCθ—deficient mice were found to be impaired in T cell-mediated immune responses, apparently, due to inability of their antigen triggered T cells to activate the AP-1 and NF-κB transcription factors (5).
KeywordsTyrosine Phosphorylation Reactive Oxygen Intermediate Induce Tyrosine Phosphorylation Critical Transcription Factor Cell Activation Response
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