PI(3,4,5)P3 potentiates phospholipase C-β activity

被引：6
作者：
Zhang, Yong [1 ,2 ]
Kwon, Sun Hyung [1 ]
Vogel, Walter K. [1 ]
Filtz, Theresa M. [1 ,2 ]
机构：
[1] Oregon State Univ, Dept Pharmaceut Sci, Corvallis, OR 97331 USA
[2] Oregon State Univ, Mol & Cellular Biol Program, Corvallis, OR 97331 USA
来源：
JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION | 2009年 / 29卷 / 01期
关键词：
Phospholipase C-beta; phosphatidylinositol 3,4,5-trisphosphate; G protein-coupled receptors; phosphatidylinositol; 3-kinase; PLECKSTRIN HOMOLOGY DOMAIN; PHOSPHATIDYLINOSITOL; 3-KINASE; ACTIVATION; RECEPTOR; PROTEIN; GAMMA; INHIBITOR; CALCIUM; MUSCLE; ASSOCIATION;
D O I：
10.1080/10799890902729449
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Phospholipase C-beta (PLC-beta) isozymes are key effectors in G protein-coupled signaling pathways. Previously, we showed that PLC-beta 1 and PLC-beta 3 bound immobilized PIP3. In this study, PIP3 was found to potentiate Ca2+-stimulated PLC-beta activities using an in vitro reconstitution assay. LY294002, a specific PI 3-kinase inhibitor, significantly inhibited 10 min of agonist-stimulated total IP accumulation. Both LY294002 and wortmannin inhibited 90 sec of agonist-stimulated IP3 accumulation in intact cells. Moreover, transfected p110CAAX, a constitutively activated PI 3-kinase catalytic subunit, increased 90 sec of oxytocin-stimulated IP 3 accumulation. Receptor-ligand binding assays indicated that LY294002 did not affect G protein-coupled receptors directly, suggesting a physiological role for PIP3 in directly potentiating PLC-beta activity. When coexpressed with p110CAAX, fluorescence-tagged PLC-beta 3 was increasingly localized to the plasma membrane. Additional observations suggest that the PH domain of PLC-beta is not important for p110CAAX-induced membrane association.
引用
收藏
页码：52 / 62
页数：11
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