Mercedes Di Bernardo, Victoria L León Guerrero, Jacob C Sutoski, William Rod Hardy, Lesley T MacNeil
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引用次数: 0
摘要
Shc 蛋白在许多不同的信号通路中发挥作用,介导依赖磷酸化的蛋白质-蛋白质相互作用。这些蛋白的特点是存在两个磷酸化酪氨酸结合域,即 N 端 PTB 和 C 端 SH2。我们描述了一种以前未被发现的秀丽隐杆线虫 Shc 基因 shc-3,并描述了它在应激反应中的作用。shc-3和shc-1都是在L1停滞期长期存活和在热应激中存活所必需的,但它们在这些过程中并不是多余的,而是扮演着不同的角色。缺失shc-3不会进一步降低daf-16突变体在L1停滞期的存活率,这表明与SHC-1一样,SHC-3也在类胰岛素信号通路中发挥作用。在 SHC-3 缺失的情况下,DAF-16 核进入和退出的速度减慢,这表明 DAF-16 信号的快速变化需要 SHC-3。
SHC-3: a previously unidentified C. elegans Shc family member functions in the insulin-like signaling pathway to enhance survival during L1 arrest.
Shc (Src homologous and collagen) proteins function in many different signaling pathways where they mediate phosphorylation-dependent protein-protein interactions. These proteins are characterized by the presence of two phosphotyrosine-binding domains, an N-terminal PTB and a C-terminal SH2. We describe a previously unrecognized Caenorhabditis elegans Shc gene, shc-3 and characterize its role in stress response. Both shc-3 and shc-1 are required for long-term survival in L1 arrest and survival in heat stress, however, they do not act redundantly but rather play distinct roles in these processes. Loss of shc-3 did not further decrease survival of daf-16 mutants in L1 arrest, suggesting that like SHC-1, SHC-3 functions in the insulin-like signaling pathway. In the absence of SHC-3, DAF-16 nuclear entry and exit are slowed, suggesting that SHC-3 is required for rapid changes in DAF-16 signaling.
期刊介绍:
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