Glucose limitation activates AMPK coupled SENP1-Sirt3 signalling in mitochondria for T cell memory development

Memory T cells are particularly reliant on fatty acid oxidation as a source of energy. Here the authors show this reliance is controlled by AMPK sensing of glucose deprivation that triggers SENP1-Sirt3 signalling, driving fatty acid oxidation and memory differentiation in T cells via deacetylation o...

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Autores principales: Jianli He, Xun Shangguan, Wei Zhou, Ying Cao, Quan Zheng, Jun Tu, Gaolei Hu, Zi Liang, Cen Jiang, Liufu Deng, Shengdian Wang, Wen Yang, Yong Zuo, Jiao Ma, Rong Cai, Yalan Chen, Qiuju Fan, Baijun Dong, Wei Xue, Hongsheng Tan, Yitao Qi, Jianmin Gu, Bing Su, Y. Eugene Chin, Guoqiang Chen, Qi Wang, Tianshi Wang, Jinke Cheng
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/102b38001d4a4513871efcad72767745
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Sumario:Memory T cells are particularly reliant on fatty acid oxidation as a source of energy. Here the authors show this reliance is controlled by AMPK sensing of glucose deprivation that triggers SENP1-Sirt3 signalling, driving fatty acid oxidation and memory differentiation in T cells via deacetylation of YME1L1 to induce mitochondrial fusion.