High Magnetic Field Laboratory, Key Laboratory of High Magnetic Field and Ion Beam Physical Biology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, P. R. China.
Medical Research Council (MRC) Protein Phosphorylation and Ubiquitylation Unit, School of Life Sciences, University of Dundee, Dundee, UK.
Autophagy. 2021 Apr;17(4):1054-1056. doi: 10.1080/15548627.2021.1898750. Epub 2021 Mar 17.
Although it has been reported that some autophagy-related proteins could regulate the cell cycle, the function of ULK1-ATG13, the only protein kinase complex in macroautophagy/autophagy, remains unclear. We recently found that mitotic ULK1 and ATG13 are both substrates of the key cell cycle regulator CDK1-CCNB/cyclin B. CDK1-induced ULK1-ATG13 phosphorylation promotes mitotic autophagy and cell cycle progression. Moreover, and double-knockout significantly inhibits cell cycle progression and tumor cell proliferation and . These findings bridge the mutual regulation between autophagic and mitotic key kinases and provide a theoretical basis for autophagy- and cell division-related diseases based on combination therapy.
虽然已经有报道称一些自噬相关蛋白可以调节细胞周期，但巨自噬/自噬中唯一的蛋白激酶复合物 ULK1-ATG13 的功能仍不清楚。我们最近发现，有丝分裂 ULK1 和 ATG13 都是关键细胞周期调节剂 CDK1-CyclinB/细胞周期蛋白 B 的底物。CDK1 诱导的 ULK1-ATG13 磷酸化促进有丝分裂自噬和细胞周期进程。此外，和双敲除显著抑制细胞周期进程和肿瘤细胞增殖。这些发现架起了自噬和有丝分裂关键激酶之间相互调节的桥梁，并为基于联合治疗的自噬和细胞分裂相关疾病提供了理论基础。
