The role of the selective adaptor p62 and ubiquitin-like proteins in autophagy.
The role of the selective adaptor p62 and ubiquitin-like proteins in autophagy.
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DOI：
10.1155/2014/832704
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发表时间：
2014
影响因子：
--
通讯作者：
Lőw P
中科院分区：
文献类型：
--
作者：
Lippai M;Lőw P
泛素-蛋白酶体系统和自噬长期以来被视为独立的、平行的降解系统，没有交叉点。到目前为止，我们知道这些降解途径共享某些底物和调节分子，并表现出协调和补偿功能。发现了两种自噬体生物发生所需的泛素样蛋白缀合途径：Atg 12-Atg 5-Atg 16和Atg 8系统。自噬一直被认为是一个基本上非选择性的过程，但事实证明它至少是部分选择性的。自噬的选择性底物包括受损的线粒体、细胞内病原体，甚至是在泛素结合自噬衔接子（如p62/SQSTM 1、NBR 1、NDP 52和Optineurin）的帮助下的胞质蛋白的子集。这些蛋白质选择性地识别自噬货物，并通过与属于Atg 8/LC 3家族的小泛素样修饰剂结合来介导其吞噬进入自噬体。
The ubiquitin-proteasome system and autophagy were long viewed as independent, parallel degradation systems with no point of intersection. By now we know that these degradation pathways share certain substrates and regulatory molecules and show coordinated and compensatory function. Two ubiquitin-like protein conjugation pathways were discovered that are required for autophagosome biogenesis: the Atg12-Atg5-Atg16 and Atg8 systems. Autophagy has been considered to be essentially a nonselective process, but it turned out to be at least partially selective. Selective substrates of autophagy include damaged mitochondria, intracellular pathogens, and even a subset of cytosolic proteins with the help of ubiquitin-binding autophagic adaptors, such as p62/SQSTM1, NBR1, NDP52, and Optineurin. These proteins selectively recognize autophagic cargo and mediate its engulfment into autophagosomes by binding to the small ubiquitin-like modifiers that belong to the Atg8/LC3 family.