胰岛素样生长因子途径对秀丽隐杆线虫外阴发育过程中MAP激酶信号的调控。

microPublication biology Pub Date : 2025-03-21 eCollection Date: 2025-01-01 DOI:10.17912/micropub.biology.001557
Matthew Eroglu, W Brent Derry
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引用次数: 0

摘要

器官发育依赖于多种信号通路协同作用来指定细胞命运。特定信号通路如EGF-Ras-MAPK的不适当活性或不活性可导致去分化和癌症。在秀丽隐杆线虫中,Ras/ let-60功能突变的获得导致多个类似肿瘤的腹侧外阴样病变的异位发展。然而,这种表型依赖于正常的胰岛素样生长因子(IGF)信号。在这里,我们探讨了IGF受体daf-2下游因子如何修饰Ras信号。这些研究使我们确定了细胞命运的调节因子,如锌指蛋白编码基因mstr-1 (F22D6.2),与哺乳动物Zfand3 / 5 / 6同源。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Regulation of MAP Kinase signaling by the insulin-like growth factor pathway during C. elegans vulval development.

Organ development depends on multiple signaling pathways working in concert to specify cell fates. Improper activity or inactivity of specific signaling pathways such as EGF-Ras-MAPK can lead to dedifferentiation and cancer. In C. elegans , gain of function mutations in Ras/ let-60 lead to ectopic development of multiple ventral vulva-like lesions resembling tumors. However, this phenotype depends on normal insulin-like growth factor (IGF) signaling. Here, we probe how factors downstream of the IGF receptor daf-2 modify Ras signaling. These investigations led us to identify regulators of cell fate such as the Zinc finger protein encoding gene mstr-1 ( F22D6.2 ), homologous to mammalian Zfand3 / 5 / 6 .

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