XBP-1 是一个细胞非自主调节器的抗压力和寿命的长寿
Rebecca C Taylor1, Andrew Dillin
1The Howard Hughes Medical Institute, University of California Berkeley, Berkeley, CA 94720, USA.
Cell
|June 25, 2013
概括
衰老会损害蛋白质稳定,但激活神经元中的XBP-1s可以恢复它. 这种神经元衍生信号通过细胞非自主UPR (ER) 激活来增强C. elegans的抗压能力和寿命.
科学领域:
- 细胞生物学 细胞生物学
- 衰老研究研究 衰老研究
- 神经科学是一个神经科学.
背景情况:
- 蛋白质稳定,维护蛋白质稳定,对于细胞功能和生物体健康至关重要.
- 老龄化导致蛋白质稳定性下降,导致与年龄相关的疾病.
- 细胞内膜网膜未展开的蛋白质反应 (UPR(ER)) 是一个关键的细胞途径,用于管理蛋白质稳定.
研究的目的:
- 调查UPR (ER) 在C. elegans衰老中的作用.
- 为了确定是否可以逆转年龄开始的蛋白质稳定性损失.
- 阐明衰老中细胞非自主信号传递的机制.
主要方法:
- 在老化的C. elegans中分析UPR (ER).
- 在神经元中表达构成性活跃的XBP-1 (XBP-1s).
- 对抗压力和长寿的评估.
- 对细胞非自主信号通路的研究.
- 评估小透明囊泡 (SCV) 的释放.
主要成果:
- 在C. elegans中,与年龄相关的ER蛋白质稳定性损失可以通过神经元XBP-1s表达来逆转.
- 神经系衍生XBP-1s拯救了抗压力,并增加了寿命.
- 在遥远的非神经元细胞中,XBP-1s通过细胞非自主机制激活了UPR(ER).
- 远端UPR (ER) 组件的损失阻碍了长寿的好处.
- 抑制SCV释放会破坏XBP-1s介导的非自主信号传递.
结论:
- 通过XBP-1s的神经元UPR (ER) 激活可以抵消与衰老相关的蛋白质稳定性下降.
- 一个细胞非自主信号通路,可能涉及神经递质,介导这些长寿益处.
- 这些发现表明,分泌的ER应激信号 (SERSS) 增强了ER应激抵抗力和寿命.
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