INSERM, U.624, Parc Scientifique de Luminy, Marseille, France.
Cancer Lett. 2010 Feb 1;288(1):116-23. doi: 10.1016/j.canlet.2009.06.030. Epub 2009 Jul 23.
ArgBP2 is a multi-adapter protein involved in signal transduction associated to the cytoskeleton and was shown to regulate the migration and adhesion of pancreatic cancer cells thereby modulating their tumorigenicity. Here we describe the interaction of ArgBP2 with CIP4, a new associated protein identified by yeast two-hybrid. We found that both proteins modulated their reciprocal tyrosine phosphorylation catalyzed by the non-receptor tyrosine kinase c-Abl. We observed that, like ArgBP2, CIP4 directly interacted with WAVE1 and could enhance its phosphorylation by c-Abl. ArgBP2 and CIP4 acted synergistically to increase WAVE1 tyrosine phosphorylation. Finally, we could show that CIP4 was dispensable for the ArgBP2 induced blockade of cell migration whereas its overexpression was deleterious for this important function of ArgBP2.
ArgBP2 是一种多接头蛋白,参与与细胞骨架相关的信号转导,已被证明可调节胰腺癌细胞的迁移和黏附,从而调节其致瘤性。在这里,我们描述了 ArgBP2 与 CIP4 的相互作用,CIP4 是通过酵母双杂交鉴定的一种新的相关蛋白。我们发现,这两种蛋白均能调节非受体酪氨酸激酶 c-Abl 催化的彼此酪氨酸磷酸化。我们观察到,与 ArgBP2 一样,CIP4 可直接与 WAVE1 相互作用,并增强 c-Abl 对其的磷酸化。ArgBP2 和 CIP4 协同作用以增加 WAVE1 的酪氨酸磷酸化。最后,我们可以表明,CIP4 对于 ArgBP2 诱导的细胞迁移阻断是可有可无的,而其过表达对于 ArgBP2 的这一重要功能是有害的。