GSE138014
Enhancing Acsl4 in absence of mTORC2/Rictor drove ß-cell dedifferentiation via inhibiting FoxO1 and promoting ROS production
We here identified Acsl4, a new target of mTORC2, could rescue the impaired ß cell proliferation, but not deficient insulin secretion induced by loss of Rictor. Overall design: ex vivo overexpression Acsl4 in ßRicKO mice