Zeng L, Sachdev P, Yan L, Chan J L, Trenkle T, McClelland M, Welsh J, Wang L H
Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Mol Cell Biol. 2000 Dec;20(24):9212-24. doi: 10.1128/MCB.20.24.9212-9224.2000.
A recently reported new member of the Vav family proteins, Vav3 has been identified as a Ros receptor protein tyrosine kinase (RPTK) interacting protein by yeast two-hybrid screening. Northern analysis shows that Vav3 has a broad tissue expression profile that is distinct from those of Vav and Vav2. Two species of Vav3 transcripts, 3.4 and 5.4 kb, were detected with a differential expression pattern in various tissues. Transient expression of Vav in 293T and NIH 3T3 cells demonstrated that ligand stimulation of several RPTKs (epidermal growth factor receptor [EGFR], Ros, insulin receptor [IR], and insulin-like growth factor I receptor [IGFR]) led to tyrosine phosphorylation of Vav3 and its association with the receptors as well as their downstream signaling molecules, including Shc, Grb2, phospholipase C (PLC-gamma), and phosphatidylinositol 3 kinase. In vitro binding assays using glutathione S-transferase-fusion polypeptides containing the GTPase-binding domains of Rok-alpha, Pak, or Ack revealed that overexpression of Vav3 in NIH 3T3 cells resulted in the activation of Rac-1 and Cdc42 whereas a deletion mutant lacking the N-terminal calponin homology and acidic region domains activated RhoA and Rac-1 but lost the ability to activate Cdc42. Vav3 induced marked membrane ruffles and microspikes in NIH 3T3 cells, while the N-terminal truncation mutants of Vav3 significantly enhanced membrane ruffle formation but had a reduced ability to induce microspikes. Activation of IR further enhanced the ability of Vav3 to induce membrane ruffles, but IGFR activation specifically promoted Vav3-mediated microspike formation. N-terminal truncation of Vav3 activated its transforming potential, as measured by focus-formation assays. We conclude that Vav3 mediates RPTK signaling and regulates GTPase activity, its native and mutant forms are able to modulate cell morphology, and it has the potential to induce cell transformation.
最近报道的Vav家族蛋白新成员Vav3,通过酵母双杂交筛选被鉴定为Ros受体蛋白酪氨酸激酶(RPTK)相互作用蛋白。Northern分析表明,Vav3具有广泛的组织表达谱,与Vav和Vav2不同。在各种组织中检测到两种Vav3转录本,3.4 kb和5.4 kb,具有差异表达模式。Vav在293T和NIH 3T3细胞中的瞬时表达表明,几种RPTK(表皮生长因子受体[EGFR]、Ros、胰岛素受体[IR]和胰岛素样生长因子I受体[IGFR])的配体刺激导致Vav3的酪氨酸磷酸化及其与受体以及它们的下游信号分子(包括Shc、Grb2、磷脂酶C[PLC-γ]和磷脂酰肌醇3激酶)的结合。使用含有Rok-α、Pak或Ack的GTP酶结合结构域的谷胱甘肽S-转移酶融合多肽进行的体外结合试验表明,NIH 3T3细胞中Vav3的过表达导致Rac-1和Cdc42的激活,而缺乏N端钙调蛋白同源性和酸性区域结构域的缺失突变体激活RhoA和Rac-1,但失去了激活Cdc42的能力。Vav3在NIH 3T3细胞中诱导明显的膜皱褶和微刺,而Vav3的N端截短突变体显著增强膜皱褶形成,但诱导微刺的能力降低。IR的激活进一步增强了Vav3诱导膜皱褶的能力,但IGFR的激活特异性促进了Vav3介导的微刺形成。通过焦点形成试验测量,Vav3的N端截短激活了其转化潜能。我们得出结论,Vav3介导RPTK信号传导并调节GTP酶活性,其天然和突变形式能够调节细胞形态,并且它具有诱导细胞转化的潜力。