Title : Phospholipase C-related but catalytically inactive protein is required for insulin-induced cell surface expression of gamma-aminobutyric acid type A receptors.

Pub. Date : 2010 Feb 12

PMID : 19996098






5 Functional Relationships(s)
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Protein Name
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1 In this study, we investigated whether phospholipase C-related but catalytically inactive protein (PRIP) is involved in insulin-induced GABA(A) receptor insertion. gamma-Aminobutyric Acid insulin Homo sapiens
2 Insulin potentiated the GABA-induced Cl(-) current (I(GABA)) by about 30% in wild-type neurons, but not in PRIP1 and PRIP2 double-knock-out (DKO) neurons, suggesting that PRIP is involved in insulin-induced potentiation. gamma-Aminobutyric Acid insulin Homo sapiens
3 Insulin potentiated the GABA-induced Cl(-) current (I(GABA)) by about 30% in wild-type neurons, but not in PRIP1 and PRIP2 double-knock-out (DKO) neurons, suggesting that PRIP is involved in insulin-induced potentiation. gamma-Aminobutyric Acid insulin Homo sapiens
4 Insulin potentiated the GABA-induced Cl(-) current (I(GABA)) by about 30% in wild-type neurons, but not in PRIP1 and PRIP2 double-knock-out (DKO) neurons, suggesting that PRIP is involved in insulin-induced potentiation. gamma-Aminobutyric Acid insulin Homo sapiens
5 The disruption of the binding between PRIP and the GABA(A) receptor beta-subunit by PRIP interference peptide attenuated the insulin potentiation of I(GABA). gamma-Aminobutyric Acid insulin Homo sapiens