Title : Protein kinase A- and C-induced insulin release from Ca2+ -insensitive pools.

Pub. Date : 2003 May

PMID : 12639716






4 Functional Relationships(s)
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1 In the present study we show that treatment of intact mouse islets and RINm5F cells with protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) or protein kinase A (PKA) activator forskolin promoted insulin secretion with no changes of [Ca(2+)](i). Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
2 In the present study we show that treatment of intact mouse islets and RINm5F cells with protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) or protein kinase A (PKA) activator forskolin promoted insulin secretion with no changes of [Ca(2+)](i). Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
3 PMA treatment caused translocation of PKC-alpha and PKC- epsilon from cytosol to membrane, implying that selectively PKC-alpha and PKC- epsilon isoforms might be important for insulin secretion. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus
4 PMA treatment caused translocation of PKC-alpha and PKC- epsilon from cytosol to membrane, implying that selectively PKC-alpha and PKC- epsilon isoforms might be important for insulin secretion. Tetradecanoylphorbol Acetate protein kinase C, alpha Rattus norvegicus