KN-93 inhibition of G protein signaling is independent of the ability of Ca2+/calmodulin-dependent protein kinase II to phosphorylate phospholipase Cβ3 on 537-Ser

Molecular and Cellular Endocrinology

Volumn 175, Issue 1-2, 2001, Pages 149-156

  Yue, Caiping ^a   Sanborn, Barbara M ^a  

^a UNIVERSITY OF TEXAS MEDICAL SCHOOL   (United States)

Author keywords

CaMK II; G protein; Phosphorylation; PI turnover; PLC

Indexed keywords

CARBACHOL; GUANINE NUCLEOTIDE BINDING PROTEIN; IONOMYCIN; KN 92; N [2 [[N [3 (4 CHLOROPHENYL) 2 PROPENYL] N METHYLAMINO]METHYL]PHENYL] N (2 HYDROXYETHYL) 4 METHOXYBENZENESULFONAMIDE; PHOSPHATIDYLINOSITIDE; PHOSPHOLIPASE C; PROTEIN KINASE (CALCIUM,CALMODULIN) II; PROTEIN KINASE INHIBITOR; UNCLASSIFIED DRUG;

ANIMAL CELL; ARTICLE; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME PURIFICATION; MUTATION; NONHUMAN; PHOSPHORYLATION; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; SITE DIRECTED MUTAGENESIS;

AMINO ACID SUBSTITUTION; ANIMALS; BENZYLAMINES; BINDING SITES; CA(2+)-CALMODULIN DEPENDENT PROTEIN KINASE; ENZYME INHIBITORS; HETEROTRIMERIC GTP-BINDING PROTEINS; ISOENZYMES; PHOSPHATIDYLINOSITOLS; PHOSPHOLIPASE C; PHOSPHORYLATION; RATS; SERINE; SIGNAL TRANSDUCTION; SULFONAMIDES; TRANSFECTION; TUMOR CELLS, CULTURED;

EID: 0035946547     PISSN: 03037207     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0303-7207(01)00383-5     Document Type: Article

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