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The G protein G alpha(13) is required for growth factor-induced cell migration

机译:G蛋白G alpha(13)是生长因子诱导的细胞迁移所必需的

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摘要

Heterotrimeric G proteins are critical cellular signal transducers. They are known to directly relay signals from seven-transmembrane G protein-coupled receptors (GPCRs) to downstream effectors. On the other hand, receptor tyrosine kinases (RTKs), a different family of membrane receptors, signal through docking sites in their carboxy-terminal tails created by autophosphorylated tyrosine residues. Here we show that a heterotrimeric G protein, G alpha(13), is essential for RTK-nduced migration of mouse fibroblast and endothelial cells. G alpha(13) activity in cell migration is retained in a C-terminal mutant that is defective in GPCR coupling, suggesting that the migration function is independent of GPCR signaling. Thus, G alpha(13) appears to be a critical signal transducer for RTKs as well as GPCRs. This broader role of G alpha(13) in cell migration initiated by two types of receptors could provide a molecular basis for the vascular system defects exhibited by G alpha(13) knockout mice.
机译:异三聚体G蛋白是关键的细胞信号转导子。已知它们可以直接将信号从七跨膜G蛋白偶联受体(GPCR)传递到下游效应子。另一方面,另一类膜受体受体酪氨酸激酶(RTK)通过自身磷酸化的酪氨酸残基在其羧基末端尾部的停靠位点发出信号。在这里,我们显示异三聚体G蛋白G alpha(13)对于RTK诱导的小鼠成纤维细胞和内皮细胞迁移至关重要。在细胞迁移中的G alpha(13)活性保留在GPCR偶联缺陷的C端突变体中,表明迁移功能独立于GPCR信号传导。因此,G alpha(13)似乎是RTK和GPCR的关键信号转换器。 G alpha(13)在由两种类型的受体引发的细胞迁移中的广泛作用可以为G alpha(13)敲除小鼠表现出的血管系统缺陷提供分子基础。

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