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Insulin and insulin-like growth factor-1 stimulate dephosphorylation of paxillin in parallel with focal adhesion kinase.胰岛素和胰岛素样生长因子-1与粘着斑激酶同时刺激桩蛋白的去磷酸化。
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2
Csk enhances insulin-stimulated dephosphorylation of focal adhesion proteins.Csk增强胰岛素刺激的粘着斑蛋白去磷酸化。
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3
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4
Opposite effects of insulin on focal adhesion proteins in 3T3-L1 adipocytes and in cells overexpressing the insulin receptor.胰岛素对3T3-L1脂肪细胞和过表达胰岛素受体的细胞中粘着斑蛋白的相反作用。
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TC-PTP dephosphorylates the guanine nucleotide exchange factor C3G (RapGEF1) and negatively regulates differentiation of human neuroblastoma cells.TC-PTP 去磷酸化鸟嘌呤核苷酸交换因子 C3G（RapGEF1），并负调控人神经母细胞瘤细胞的分化。
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7
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8
Opposite effects of insulin on focal adhesion proteins in 3T3-L1 adipocytes and in cells overexpressing the insulin receptor.胰岛素对3T3-L1脂肪细胞和过表达胰岛素受体的细胞中粘着斑蛋白的相反作用。
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9
Insulin stimulates the tyrosine dephosphorylation of docking protein p130cas (Crk-associated substrate), promoting the switch of the adaptor protein crk from p130cas to newly phosphorylated insulin receptor substrate-1.胰岛素刺激对接蛋白p130cas（Crk相关底物）的酪氨酸去磷酸化，促使衔接蛋白crk从p130cas转换至新磷酸化的胰岛素受体底物-1。
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本文引用的文献

1
Purified hybrid insulin/insulin-like growth factor-I receptors bind insulin-like growth factor-I, but not insulin, with high affinity.纯化的杂合胰岛素/胰岛素样生长因子-I受体以高亲和力结合胰岛素样生长因子-I，但不结合胰岛素。
Biochem J. 1993 Mar 1;290 ( Pt 2)(Pt 2):419-26. doi: 10.1042/bj2900419.
2
Tyrosine phosphorylation of the focal adhesion kinase pp125FAK during development: relation to paxillin.发育过程中粘着斑激酶pp125FAK的酪氨酸磷酸化：与桩蛋白的关系。
J Cell Sci. 1993 Jul;105 ( Pt 3):637-45. doi: 10.1242/jcs.105.3.637.
3
Bombesin stimulation of p125 focal adhesion kinase tyrosine phosphorylation. Role of protein kinase C, Ca2+ mobilization, and the actin cytoskeleton.蛙皮素刺激p125粘着斑激酶酪氨酸磷酸化。蛋白激酶C、钙离子动员及肌动蛋白细胞骨架的作用。
J Biol Chem. 1993 Jul 5;268(19):14261-8.
4
Platelet-derived growth factor modulation of focal adhesion kinase (p125FAK) and paxillin tyrosine phosphorylation in Swiss 3T3 cells. Bell-shaped dose response and cross-talk with bombesin.血小板衍生生长因子对瑞士3T3细胞中粘着斑激酶（p125FAK）和桩蛋白酪氨酸磷酸化的调节。钟形剂量反应以及与蛙皮素的相互作用。
J Biol Chem. 1994 Jan 7;269(1):704-10.
5
Role of the carboxyl-terminal domains of the insulin and insulin-like growth factor I receptors in receptor function.胰岛素及胰岛素样生长因子I受体的羧基末端结构域在受体功能中的作用。
J Biol Chem. 1994 May 13;269(19):13922-8.
6
Insulin receptor autophosphorylation and exogenous substrate phosphorylation: role of receptor C-terminus and effects of mild reduction.
Biochem Biophys Res Commun. 1994 Apr 15;200(1):330-7. doi: 10.1006/bbrc.1994.1452.
7
Insulin stimulates the tyrosine dephosphorylation of pp125 focal adhesion kinase.胰岛素刺激pp125粘着斑激酶的酪氨酸去磷酸化。
J Biol Chem. 1995 Jan 20;270(3):991-4. doi: 10.1074/jbc.270.3.991.
8
Insulin action and the insulin signaling network.胰岛素作用与胰岛素信号网络。
Endocr Rev. 1995 Apr;16(2):117-42. doi: 10.1210/edrv-16-2-117.
9
Signal transduction through integrins: a central role for focal adhesion kinase?整合素介导的信号转导：黏着斑激酶起核心作用？
Bioessays. 1995 Mar;17(3):229-36. doi: 10.1002/bies.950170309.
10
Activation of the small GTP-binding proteins rho and rac by growth factor receptors.生长因子受体对小GTP结合蛋白rho和rac的激活作用。
J Cell Sci. 1995 Jan;108 ( Pt 1):225-33. doi: 10.1242/jcs.108.1.225.

胰岛素和胰岛素样生长因子-1与粘着斑激酶同时刺激桩蛋白的去磷酸化。

Insulin and insulin-like growth factor-1 stimulate dephosphorylation of paxillin in parallel with focal adhesion kinase.

作者信息

Konstantopoulos N, Clark S

机构信息

University of Melbourne, Department of Medicine, Parkville, Victoria, Australia.

出版信息

Biochem J. 1996 Mar 1;314 ( Pt 2)(Pt 2):387-90. doi: 10.1042/bj3140387.

DOI:10.1042/bj3140387
PMID:8670044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1217059/
Abstract

Paxillin and focal adhesion kinase (pp125FAK) co-localize in focal adhesions; recently insulin has been shown to stimulate the dephosphorylation of pp125FAK; however, its effect on paxillin is unknown. We show that insulin and IGF-1 can stimulate the dephosphorylation of paxillin in CHOT (overexpress human insulin receptors) and CHO delta CT69 (overexpress insulin receptors lacking C-terminal 69 amino acids) cells. Furthermore, the insulin-receptor C-terminus is not needed for either insulin or IGF-1 to stimulate paxillin or pp125FAK dephosphorylation in the CHO (Chinese-hamster ovary) cell lines used.

摘要

桩蛋白和粘着斑激酶（pp125FAK）共定位于粘着斑；最近有研究表明胰岛素可刺激pp125FAK的去磷酸化；然而，其对桩蛋白的影响尚不清楚。我们发现胰岛素和胰岛素样生长因子-1（IGF-1）可刺激CHOT（过表达人胰岛素受体）细胞和CHOδCT69（过表达缺失C末端69个氨基酸的胰岛素受体）细胞中桩蛋白的去磷酸化。此外，在所使用的CHO（中国仓鼠卵巢）细胞系中，胰岛素或IGF-1刺激桩蛋白或pp125FAK去磷酸化并不需要胰岛素受体的C末端。