Enhancing Acsl4 in absence of mTORC2/Rictor drove Ã-cell dedifferentiation via inhibiting FoxO1 and promoting ROS production
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https://www.ncbi.nlm.nih.gov/sra/SRP223227
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资源简介：
We here identified Acsl4, a new target of mTORC2, could rescue the impaired à cell proliferation, but not deficient insulin secretion induced by loss of Rictor. Overall design: ex vivo overexpression Acsl4 in ÃRicKO mice
创建时间：
2022-12-31
