The peroxisome as a cell signaling organelle.

The peroxisome as a cell signaling organelle.
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DOI:
10.1016/j.ceb.2016.02.017
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发表时间:
2016-04
影响因子:
7.5
通讯作者:
Walker CL
Walker CL
中科院分区:
生物学2区
文献类型:
--
作者:
Tripathi DN;Walker CL

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过氧化物酶体参与脂质代谢,是细胞中ROS的主要来源。它们在细胞能量平衡和氧化还原稳态中的重要性是公认的,正如需要维持过氧化物酶体稳态以防止与这些细胞器过少或过多相关的病理一样。细胞如何调节过氧化物酶体的数量仍然有些难以捉摸。最近,调节mTORC1信号的肿瘤抑制因子ATM和TSC已经定位于过氧化物酶体。当被过氧化物酶体ROS激活时,ATM向TSC发出信号,抑制mTORC1信号,增加细胞内的自噬通量,并磷酸化过氧化物酶体蛋白PEX 5,靶向过氧化物酶体进行选择性自噬(pexophagy),提供了一种利用ROS作为变阻器调节过氧化物酶体稳态的机制。
Peroxisomes participate in lipid metabolism, and are a major source of ROS in the cell. Their importance in cellular energy balance and redox homeostasis is well-established, as is the need to maintain peroxisome homeostasis to prevent pathologies associated with too few, or too many, of these organelles. How cells regulate peroxisome number has remained somewhat elusive. Recently, the tumor suppressors ATM and TSC, which regulate mTORC1 signaling, have been localized to peroxisomes. When activated by peroxisomal ROS, ATM signals to TSC to repress mTORC1 signaling and increase autophagic flux in cells, and also phosphorylates the peroxisomal protein PEX 5 to target peroxisomes for selective autophagy (pexophagy), providing a mechanism for regulation of peroxisomal homeostasis using ROS as a rheostat.
各种细胞内病原体激活过氧化物酶体的III型干扰素表达。
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