人类自噬起始复合物ULK1C和PI3KC3-C1。
The human autophagy-initiating complexes ULK1C and PI3KC3-C1.
作者信息
Chen Minghao, Hurley James H
机构信息
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA; California Institute for Quantitative Biosciences, University of California, Berkeley, Berkeley, California, USA; Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, Maryland, USA.
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA; California Institute for Quantitative Biosciences, University of California, Berkeley, Berkeley, California, USA; Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, Maryland, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, California, USA.
出版信息
J Biol Chem. 2025 Jun 19;301(7):110391. doi: 10.1016/j.jbc.2025.110391.
The unc-51-like kinase complex (ULK1C) and the class III phosphatidylinositol 3-kinase complex I (PI3KC3-C1) are the key regulators of macroautophagy initiation. Understanding the assembly and coordination of these two complexes is essential for deciphering their cellular regulation and targeting them for therapeutic enhancement. This review highlights recent advances in our understanding of the structural organization and activation mechanisms of ULK1C and PI3KC3-C1 at the molecular level and discusses their roles within the protein interaction network governing autophagy initiation.
UNC-51样激酶复合物（ULK1C）和III类磷脂酰肌醇3-激酶复合物I（PI3KC3-C1）是自噬起始的关键调节因子。了解这两种复合物的组装和协调对于解读它们的细胞调控机制以及将它们作为治疗增强靶点至关重要。本综述重点介绍了我们在分子水平上对ULK1C和PI3KC3-C1的结构组织和激活机制的最新认识进展，并讨论了它们在控制自噬起始的蛋白质相互作用网络中的作用。
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