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AMBRA1通过一条不依赖自噬相关蛋白7(ATG7)的途径参与T细胞受体介导的代谢重编程。

AMBRA1 is involved in T cell receptor-mediated metabolic reprogramming through an ATG7-independent pathway.

作者信息

Akatsuka Hisako, Kuga Shuhei, Masuhara Kaori, Davaadorj Odontuya, Okada Chisa, Iida Yumi, Okada Yoshinori, Fukunishi Nahoko, Suzuki Takahiro, Hosomichi Kazuyoshi, Ohtsuka Masato, Tanaka Masafumi, Inoue Ituro, Kimura Minoru, Sato Takehito

机构信息

Department of Host Defense Mechanism, Japan; Department of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Japan.

Department of Host Defense Mechanism, Japan.

出版信息

Biochem Biophys Res Commun. 2017 Sep 30;491(4):1098-1104. doi: 10.1016/j.bbrc.2017.08.019. Epub 2017 Aug 5.

DOI:10.1016/j.bbrc.2017.08.019
PMID:28789945
Abstract

Metabolic reprogramming contributes to dynamic alteration of cell functions and characteristics. In T cells, TCR-mediated signaling evokes metabolic reprogramming and autophagy. AMBRA1 is known to serve in the facilitation of autophagy and quality control of mitochondria, but the role of AMBRA1 in T cell metabolic alteration is unknown. Here, we show that AMBRA1, but not ATG7, plays a role in TCR-mediated control of glycolytic factors and mitochondrial mass, while both AMBRA1 and ATG7 are required for autolysosome formation. Our results suggested that AMBRA1 is a core factor that controls both autophagy and metabolic regulation.

摘要

代谢重编程有助于细胞功能和特性的动态改变。在T细胞中,TCR介导的信号传导引发代谢重编程和自噬。已知AMBRA1有助于自噬和线粒体质量控制,但AMBRA1在T细胞代谢改变中的作用尚不清楚。在这里,我们表明,AMBRA1而非ATG7在TCR介导的糖酵解因子和线粒体质量控制中发挥作用,而AMBRA1和ATG7都是自溶酶体形成所必需的。我们的结果表明,AMBRA1是控制自噬和代谢调节的核心因子。

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