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血小板衍生生长因子α受体中酪氨酸720的磷酸化是Grb2和SHP-2结合所必需的,但不是Ras激活或细胞增殖所必需的。

Phosphorylation of tyrosine 720 in the platelet-derived growth factor alpha receptor is required for binding of Grb2 and SHP-2 but not for activation of Ras or cell proliferation.

作者信息

Bazenet C E, Gelderloos J A, Kazlauskas A

机构信息

Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206, USA.

出版信息

Mol Cell Biol. 1996 Dec;16(12):6926-36. doi: 10.1128/MCB.16.12.6926.

Abstract

Following binding of platelet-derived growth factor (PDGF), the PDGF alpha receptor (alphaPDGFR) becomes tyrosine phosphorylated and associates with a number of signal transduction molecules, including phospholipase Cgamma-1 (PLCgamma-1), phosphatidylinositol 3-kinase (PI3K), the phosphotyrosine phosphatase SHP-2, Grb2, and Src. Here, we present data identifying a novel phosphorylation site in the kinase insert domain of the alphaPDGFR at tyrosine (Y) 720. We replaced this residue with phenylalanine and expressed the mutated receptor (F720) in Patch fibroblasts that do not express the alphaPDGFR. Characterization of the F720 mutant indicated that binding of two proteins, SHP-2 and Grb2, was severely impaired, whereas PLCgamma-1 and PI3K associated to wild-type levels. In addition, mutating Y720 to phenylalanine dramatically reduced PDGF-dependent tyrosine phosphorylation of SHP-2. Since Y720 was required for recruitment of two proteins, we investigated the mechanism by which these two proteins associated with the alphaPDGFR. SHP-2 bound the alphaPDGFR directly, whereas Grb2 associated indirectly, most probably via SHP-2, as Grb2 and SHP-2 coimmunoprecipitated when SHP-2 was tyrosine phosphorylated. We also compared the ability of the wild-type and F720 alphaPDGFRs to mediate a number of downstream events. Preventing the alphaPDGFR from recruiting SHP-2 and Grb2 did not compromise PDGF-AA-induced activation of Ras, initiation of DNA synthesis, or growth of cells in soft agar. We conclude that phosphorylation of the alphaPDGFR at Y720 is required for association of SHP-2 and Grb2 and tyrosine phosphorylation of SHP-2; however, these events are not required for the alphaPDGFR to activate Ras or initiate a proliferative response. In addition, these findings reveal that while SHP-2 binds to both of the receptors, it binds in different locations: to the carboxy terminus of the betaPDGFR but to the kinase insert of the alphaPDGFR.

摘要

血小板衍生生长因子(PDGF)结合后,PDGFα受体(αPDGFR)发生酪氨酸磷酸化,并与多种信号转导分子结合,包括磷脂酶Cγ-1(PLCγ-1)、磷脂酰肌醇3激酶(PI3K)、磷酸酪氨酸磷酸酶SHP-2、Grb2和Src。在此,我们展示了确定αPDGFR激酶插入结构域中酪氨酸(Y)720处一个新的磷酸化位点的数据。我们将该残基替换为苯丙氨酸,并在不表达αPDGFR的Patch成纤维细胞中表达突变受体(F720)。F720突变体的特征表明,SHP-2和Grb2这两种蛋白的结合严重受损,而PLCγ-1和PI3K的结合水平与野生型相当。此外,将Y720突变为苯丙氨酸显著降低了PDGF依赖的SHP-2酪氨酸磷酸化。由于Y720是这两种蛋白募集所必需的,我们研究了这两种蛋白与αPDGFR结合的机制。SHP-2直接结合αPDGFR,而Grb2间接结合,很可能是通过SHP-2,因为当SHP-2酪氨酸磷酸化时,Grb2和SHP-2会共同免疫沉淀。我们还比较了野生型和F720αPDGFR介导多种下游事件的能力。阻止αPDGFR募集SHP-2和Grb2并不影响PDGF-AA诱导的Ras激活、DNA合成起始或软琼脂中细胞的生长。我们得出结论,αPDGFR在Y720处的磷酸化是SHP-2和Grb2结合以及SHP-2酪氨酸磷酸化所必需的;然而,这些事件对于αPDGFR激活Ras或引发增殖反应并非必需。此外,这些发现揭示,虽然SHP-2与两种受体都结合,但结合位置不同:与βPDGFR的羧基末端结合,但与αPDGFR的激酶插入结构域结合。

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