Regulation of IkB alpha phosphorylation by PKC- and Ca(2+)-dependent signal transduction pathways.

摘要: The Ca(2+)-dependent phosphatase calcineurin, a target of FK506 and CsA, synergizes with PKC-induced activation nuclear factor (NF)-kappa B in T cell lines. We have investigated whether this synergy is present other types the mechanism(s) by which these two pathways lead to NF-kappa activation. While types, monocytic line U937 calcineurin also sufficient activate B. Having previously shown that Ca(2+)- PKC-dependent synergize accelerating degradation IkB alpha, we focused on regulation alpha phosphorylation. sequentially result phosphorylation an incomplete lines, co-activation accelerates rate results its complete degradation. Activation alone do not and/or Jurkat or cells. Treatment cells selective PKC inhibitor GF109203X abrogates PMA-induced phosphorylation/degradation irrespective pathways, but induced TNF-alpha, PKC-independent stimulus. Contrary interaction PKC, TNF-alpha at level phosphorylation, These indicate including participate specific fashion -independent