选择性自的V-ATPase依赖的诱导
Yuxiang Huang1, Dimitra Dialynaki1, Yuchen Lei1
1Life Sciences Institute and Department of Molecular, Cellular and Development Biology, University of Michigan, Ann Arbor, MI, USA.
Nature communications
|September 26, 2025
概括
空腔类型的H+转位ATPase (V-ATPase) 功能障碍激活了一个独特的自途径. 托代谢通过核糖体生物发生和NAD+合成抑制了这种V-ATPase依赖的自.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 真空类型的H+转位ATPase (V-ATPase) 通常被认为是自过程中必不可少的.
- 与卵泡淋巴瘤相关的V-ATPase突变导致溶酶脱酸和自的增加,尽管机制尚不清楚.
研究的目的:
- 阐明V-ATPase功能障碍激活自的机制.
- 为了研究这种新型V-ATPase依赖的自道的调节.
主要方法:
- 在酵母中进行转录和蛋白质分析.
- 全基因组抑制器查.
- 分析托代谢及其作用因子.
主要成果:
- V-ATPase功能障碍诱导了选择性的自流,称为V-ATPase依赖的自,与饥饿诱导的自不同.
- 托代谢通过两个途径负面调节V-ATPase依赖的自.
- 托代谢通过激活核糖体生物生成来抑制Gcn4/ATF4转化,并通过推动NAD+生物合成来抑制自.
结论:
- 维-ATPase功能障碍激活了一种独特的自途径,该途径由托代谢调节.
- 这一途径为患有V-ATPase突变的卵泡淋巴瘤患者的自性升高提供了机制性的解释.
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