CaMKII-mediated Beclin 1 phosphorylation regulates autophagy that promotes degradation of ID and neuroblastoma cell differentiation
Publication in refereed journal

香港中文大學研究人員
替代計量分析
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其它資訊
摘要Autophagy is a degradative pathway that delivers cellular components to the lysosome for degradation. The role of autophagy in cell differentiation is poorly understood. Here we show that CaMKII can directly phosphorylate Beclin 1 at Ser90 to promote K63-linked ubiquitination of Beclin 1 and activation of autophagy. Meanwhile, CaMKII can also promote K63-linked ubiquitination of inhibitor of differentiation 1/2 (Id-1/2) by catalyzing phosphorylation of Id proteins and recruiting TRAF-6. Ubiquitinated Id-1/Id-2 can then bind to p62 and be transported to autolysosomes for degradation. Id degradation promotes the differentiation of neuroblastoma cells and reduces the proportion of stem-like cells. Our study proposes a mechanism by which autophagic degradation of Id proteins can regulate cell differentiation. This suggests that targeting of CaMKII and the regulation of autophagic degradation of Id may be an effective therapeutic strategy to induce cell differentiation in neuroblastoma.
著者Xuan Li, Xiao-Qi Wu, Rong Deng, Dan-Dan Li, Jun Tang, Wen-Dan Chen, Jing-Hong Chen, Jiao Ji, Lin Jiao, Shan Jiang, Fen Yang, Gong-Kan Feng, Ravichandran Senthilkumar, Fei Yue, Hai-Liang Zhang, Rui-Yan Wu, Yan Yu, Xue-Lian Xu, Jia Mai, Zhi-Ling Li, Xiao-Dan Peng, Yun Huang, Xiang Huang, Ning-Fang Ma, Qian Tao, Yi-Xin Zeng, Xiao-Feng Zhu
期刊名稱Nature Communications
出版年份2017
月份10
日期27
卷號8
頁次1159
國際標準期刊號2041-1723
語言美式英語

上次更新時間 2021-19-01 於 02:11