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1
Phospholipase Cgamma1 negatively regulates growth hormone signalling by forming a ternary complex with Jak2 and protein tyrosine phosphatase-1B.磷脂酶Cγ1通过与Jak2和蛋白酪氨酸磷酸酶-1B形成三元复合物来负向调节生长激素信号传导。
Nat Cell Biol. 2006 Dec;8(12):1389-97. doi: 10.1038/ncb1509. Epub 2006 Nov 26.
2
Intramolecular regulation of phospholipase C-gamma1 by its C-terminal Src homology 2 domain.磷脂酶C-γ1的C末端Src同源2结构域对其进行的分子内调控。
Mol Cell Biol. 2007 Feb;27(3):854-63. doi: 10.1128/MCB.01400-06. Epub 2006 Nov 20.
3
Pleckstrin homology domain of phospholipase C-gamma1 directly binds to 68-kDa neurofilament light chain.磷脂酶C-γ1的普列克底物蛋白同源结构域直接与68 kDa神经丝轻链结合。
Exp Mol Med. 2006 Jun 30;38(3):265-72. doi: 10.1038/emm.2006.32.
4
Intramolecular interaction between phosphorylated tyrosine-783 and the C-terminal Src homology 2 domain activates phospholipase C-gamma1.磷酸化的酪氨酸-783与C端Src同源2结构域之间的分子内相互作用激活磷脂酶C-γ1。
Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4276-81. doi: 10.1073/pnas.0409590102. Epub 2005 Mar 11.
5
Point mutations in the split PLC-gamma1 PH domain modulate phosphoinositide binding.分裂型PLC-γ1 PH结构域中的点突变调节磷酸肌醇结合。
J Biochem Mol Biol. 2004 Nov 30;37(6):720-5. doi: 10.5483/bmbrep.2004.37.6.720.
6
Pleckstrin homology domains of phospholipase C-gamma1 directly interact with beta-tubulin for activation of phospholipase C-gamma1 and reciprocal modulation of beta-tubulin function in microtubule assembly.磷脂酶C-γ1的普列克底物蛋白同源结构域直接与β-微管蛋白相互作用，以激活磷脂酶C-γ1并对微管组装中β-微管蛋白的功能进行相互调节。
J Biol Chem. 2005 Feb 25;280(8):6897-905. doi: 10.1074/jbc.M406350200. Epub 2004 Dec 5.
7
Mechanism of tyrosine phosphorylation and activation of phospholipase C-gamma 1. Tyrosine 783 phosphorylation is not sufficient for lipase activation.酪氨酸磷酸化及磷脂酶C-γ1激活的机制。酪氨酸783磷酸化不足以激活脂肪酶。
J Biol Chem. 2004 Jul 30;279(31):32181-90. doi: 10.1074/jbc.M405116200. Epub 2004 May 25.
8
Regulation of phospholipase C-gamma1 by protein kinase A-dependent phosphorylation.蛋白激酶A依赖性磷酸化对磷脂酶C-γ1的调节
Adv Enzyme Regul. 2002;42:195-211. doi: 10.1016/s0065-2571(01)00031-0.
9
Interaction of elongation factor-1alpha and pleckstrin homology domain of phospholipase C-gamma 1 with activating its activity.延伸因子-1α与磷脂酶C-γ1的普列克底物蛋白同源结构域相互作用并激活其活性。
J Biol Chem. 2002 May 31;277(22):19697-702. doi: 10.1074/jbc.M111206200. Epub 2002 Mar 8.
10
Regulation of phosphoinositide-specific phospholipase C.磷酸肌醇特异性磷脂酶C的调节
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在表皮生长因子刺激下，PCL-gamma1（Y509A/F510A）中的双点突变增强了 Y783 的磷酸化和肌醇磷脂水解活性。

A double point mutation in PCL-gamma1 (Y509A/F510A) enhances Y783 phosphorylation and inositol phospholipid-hydrolyzing activity upon EGF stimulation.

机构信息

Department of Life Science, College of Natural Science, Daejin University, Pocheon 487-711, Korea.

出版信息

Exp Mol Med. 2010 Mar 31;42(3):216-27. doi: 10.3858/emm.2010.42.3.023.

DOI:10.3858/emm.2010.42.3.023
PMID:20164676
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2845006/
Abstract

Growth factor stimulation induces Y783 phosphorylation of phosphoinositide-specific PLC-gamma1, and the subsequent activation of this enzyme in a cellular signaling cascade. Previously, we showed that a double point mutation, Y509A/F510A, of PLC-gamma1, abolished interactions with translational elongation factor 1-alpha. Here, we report that the Y509A/F510A mutant PLC-gamma1 displayed extremely high levels of Y783 phosphorylation and enhanced catalytic activity, compared to wild-type PLC-gamma1, upon treatment of COS7 cells with EGF. In quiescent COS7 cells, the Y509A/F510A mutant PLC-gamma1 exhibited a constitutive hydrolytic activity, whereas the wild-type counterpart displayed a basal level of activity. Upon treatment of COS7 cells with EGF, the Y783F mutation in Y509A/F510A PLC-gamma1 (Y509A/F510A/Y783F triple mutant) cells also led to an enhanced catalytic activity, whereas Y783F mutation alone displayed a basal level of activity. Our results collectively suggest that the Y509A/F510A mutant is more susceptible to receptor tyrosine kinase-induced Y783 phosphorylation than is wild-type PLC-gamma1, but no longer requires Y783 phosphorylation step for the Y509A/F510A mutant PLC-gamma1 activation in vivo.

摘要

生长因子刺激诱导磷酯酶 C-γ1 的 Y783 磷酸化，随后在细胞信号级联中激活该酶。先前，我们表明 PLC-γ1 的 Y509A/F510A 双点突变消除了与翻译延伸因子 1-α的相互作用。在这里，我们报告说，与野生型 PLC-γ1 相比，在用 EGF 处理 COS7 细胞后，Y509A/F510A 突变型 PLC-γ1 的 Y783 磷酸化水平极高，并增强了催化活性。在静止的 COS7 细胞中，Y509A/F510A 突变型 PLC-γ1 表现出组成型水解活性，而野生型 PLC-γ1 则表现出基础水平的活性。在用 EGF 处理 COS7 细胞后，Y509A/F510A PLC-γ1 中的 Y783F 突变（Y509A/F510A/Y783F 三重突变体）也导致催化活性增强，而 Y783F 突变本身则表现出基础水平的活性。我们的结果共同表明，与野生型 PLC-γ1 相比，Y509A/F510A 突变体更容易受到受体酪氨酸激酶诱导的 Y783 磷酸化，但对于体内的 Y509A/F510A 突变型 PLC-γ1 激活，不再需要 Y783 磷酸化步骤。