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首页> 外文期刊>Molecular and Cellular Biology >Asef2 Functions as a Cdc42 Exchange Factor and Is Stimulated by the Release of an Autoinhibitory Module from a Concealed C-Terminal Activation Element
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Asef2 Functions as a Cdc42 Exchange Factor and Is Stimulated by the Release of an Autoinhibitory Module from a Concealed C-Terminal Activation Element

机译：Asef2充当Cdc42交换因子，并通过隐蔽的C末端激活元件释放自抑制模块而受到刺激

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摘要

Asef (herein called Asef1) was identified as a Rac1-specific exchange factor stimulated by adenomatous polyposis coli (APC), contributing to colorectal cancer cell metastasis. We investigated Asef2, an Asef1 homologue having a similar N-terminal APC binding region (ABR) and Src-homology 3 (SH3) domain. Contrary to previous reports, we found that Asef1 and Asef2 exchange activity is Cdc42 specific. Moreover, the ABR of Asef2 did not function independently but acted in tandem with the SH3 domain to bind APC. The ABRSH3 also bound the C-terminal tail of Asef2, allowing it to function as an autoinhibitory module within the protein. Deletion of the C-terminal tail did not constitutively activate Asef2 as predicted; rather, a conserved C-terminal segment was required for augmented Cdc42 GDP/GTP exchange. Thus, Asef2 activation involves APC releasing the ABRSH3 from the C-terminal tail, resulting in Cdc42 exchange. These results highlight a novel exchange factor regulatory mechanism and establish Asef1 and Asef2 as Cdc42 exchange factors, providing a more appropriate context for understanding the contribution of APC in establishing cell polarity and migration.
机译：Asef（以下简称Asef1）被鉴定为腺瘤性息肉病大肠杆菌（APC）刺激的Rac1特异性交换因子，有助于大肠癌细胞的转移。我们研究了Asef2，这是具有相似N末端APC结合区（ABR）和Src同源3（SH3）域的Asef1同源物。与以前的报告相反，我们发现Asef1和Asef2交换活动是Cdc42特定的。此外，Asef2的ABR并非独立运行，而是与SH3域协同作用以结合APC。 ABRSH3还结合了Asef2的C末端尾巴，从而使其可以作为蛋白质中的自抑制模块。 C末端尾部的缺失并未如预期的那样组成性地激活Asef2。相反，增加Cdc42 GDP / GTP交换需要一个保守的C末端片段。因此，Asef2激活涉及APC从C末端尾部释放ABRSH3，从而导致Cdc42交换。这些结果突出了一种新颖的交换因子调节机制，并将Asef1和Asef2建立为Cdc42交换因子，为理解APC在建立细胞极性和迁移中的作用提供了更合适的背景。

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