Title : Recovery of gap junctional intercellular communication after phorbol ester treatment requires proteasomal degradation of protein kinase C.

Pub. Date : 2003 Jul

PMID : 12807762






9 Functional Relationships(s)
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1 Treatment of cells with TPA results in the activation and subsequent depletion of the TPA-responsive protein kinase C (PKC) isoforms. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
2 Treatment of cells with TPA results in the activation and subsequent depletion of the TPA-responsive protein kinase C (PKC) isoforms. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
3 Prolonged TPA treatment induced down-regulation of PKCalpha, delta and epsilon and a reduction in the total PKC activity, which was associated with recovery of GJIC. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
4 Prolonged TPA treatment induced down-regulation of PKCalpha, delta and epsilon and a reduction in the total PKC activity, which was associated with recovery of GJIC. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
5 Co-treatment of IAR20 cells with TPA and the proteasomal inhibitor MG132 suppressed down-regulation of PKCalpha, delta and epsilon and caused prolonged PKC activity. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
6 Co-treatment of IAR20 cells with TPA and the proteasomal inhibitor MG132 suppressed down-regulation of PKCalpha, delta and epsilon and caused prolonged PKC activity. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
7 The general PKC inhibitor GF109203X reversed the effect of MG132, indicating that the prolonged TPA-induced inhibition of GJIC caused by MG132 was due to the prolonged PKC activity. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
8 The general PKC inhibitor GF109203X reversed the effect of MG132, indicating that the prolonged TPA-induced inhibition of GJIC caused by MG132 was due to the prolonged PKC activity. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
9 These results indicate that proteasomal degradation of PKC is one mechanism by which the recovery of GJIC after TPA treatment is regulated. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus