Yu Qiujing, Wang Ting, Jiang Yuhui
The Institute of Cell Metabolism, Shanghai Key Laboratory of Pancreatic Disease, Shanghai General Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Mol Cell Oncol. 2018 May 16;5(4):e1363848. doi: 10.1080/23723556.2017.1363848. eCollection 2018.
Our recent study shows that AMPK normally phosphorates fumarase (FH) at Ser75 under glucose deprivation, resulting in FH-ATF2 complex formation that facilitates transcription for cell growth arrest. Meanwhile, O-GlcNAc transferase can compete with AMPK to O-GlcNAcylate FH. In tumor cells, FH is highly O-GlcNAcylated and is proinhibited from AMPK-ATF2 signaling.
我们最近的研究表明,在葡萄糖缺乏的情况下,AMPK通常会在丝氨酸75位点磷酸化富马酸酶(FH),导致FH-ATF2复合物形成,从而促进细胞生长停滞的转录。同时,O-连接的N-乙酰葡糖胺转移酶可以与AMPK竞争,使FH发生O-连接的N-乙酰葡糖胺化。在肿瘤细胞中,FH高度O-连接的N-乙酰葡糖胺化,并且被抑制参与AMPK-ATF2信号传导。