Chinese scholars have found that phosphorylated p38α plays an important role in cell survival in proteasome injury.

Chinese scholars have found that phosphorylated p38α plays an important role in cell survival in proteasome injury.

December 22, 2016 Source: Bio Valley

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Recently, Molecular Neurobiology, an important international academic journal of neurobiology, published the latest research results of the research group of the Chinese Academy of Sciences Shanghai Institute of Life Sciences/Shanghai Jiaotong University School of Medicine Health Science Research Institute "A Central Role for Phosphorylated p38α in Linking Proteasome Inhibition -Induced Apoptosis and Autophagy", reveals an important role of phosphorylated p38α in cell survival in proteasome damage.

Autophagy and the ubiquitin proteasome system are two important protein degradation pathways in the body that cooperate with each other during apoptosis. Ubiquitin proteasome damage activates autophagy and reduces apoptosis. Therefore, studying the relationship between autophagy and apoptosis induced by proteasome injury, and the key factors between them are the hotspots of international research on the pathogenesis and treatment of protein homeostasis.

Dr. Guo Fang, a member of the Le Weidong research group, found that phosphorylated p38α can regulate autophagy and affect apoptosis in the process of proteasome injury. By inhibiting the phosphorylation of p38α, the autophagy marker protein LC3-II protein level is elevated, while the autophagy substrate SQSTM1 protein level is decreased, indicating that phosphorylation of p38α negatively regulates autophagy; further studies have found that inhibition of p38α phosphorylation can be inhibited The mTOR pathway thus activates autophagy. Activated autophagy reduces apoptosis.

This study illustrates the important role of phosphorylated p38α in autophagy and apoptosis in the proteasome injury model, providing new insights into the relationship between autophagy and apoptosis. At the same time, the study also provides a new molecular target for autophagy activation and apoptosis.

This research has been funded by the National Natural Science Foundation of China and the Chinese Academy of Sciences.

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