蛋白质毒性
高铁F1
秀丽隐杆线虫
细胞生物学
生物
热冲击系数
转录因子
热冲击
基因敲除
热休克蛋白
生长因子
细胞应激反应
胰岛素样生长因子
热休克蛋白70
战斗或逃跑反应
遗传学
蛋白质聚集
基因
受体
作者
Yuli Volovik,Lorna Moll,Filipa Marques,Moria Maman,Michal Bejerano‐Sagie,Ehud Cohen
出处
期刊:Cell Reports
[Elsevier]
日期:2014-12-01
卷期号:9 (6): 2192-2205
被引量:38
标识
DOI:10.1016/j.celrep.2014.11.028
摘要
In the nematode Caenorhabditis elegans, insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) reduction hyperactivates the transcription factors DAF-16 and heat shock factor 1 (HSF-1), creating long-lived, stress-resistant worms that are protected from proteotoxicity. How DAF-16 executes its distinct functions in response to IIS reduction is largely obscure. Here, we report that NHL-1, a member of the TRIM-NHL protein family, acts in chemosensory neurons to promote stress resistance in distal tissues by DAF-16 activation but is dispensable for the activation of HSF-1. The expression of nhl-1 is regulated by the IIS, defining a neuronal regulatory circuit that controls the organismal stress response. The knockdown of nhl-1 protects nematodes that express the Alzheimer-disease-associated Aβ peptide from proteotoxicity but has no effect on lifespan. Our findings indicate that DAF-16- and HSF-1-regulated heat-responsive mechanisms are differentially controlled by neurons and show that one neuronal protein can be involved in the activation of different stress responses in remote tissues.
科研通智能强力驱动
Strongly Powered by AbleSci AI