mTORC1-signaling switches megalin function from endocytosis to cell cycle progression

Abstract Mechanistic target of rapamycin (mTOR) signaling pathway controls eukaryotic growth by regulating metabolism, translation, autophagy and cell cycle. Genetic deletion of renal mTORC1 led to a Fanconi-like syndrome with reduction of the renal cortex, tubular epithelial transport and perturbation of the endocytic machinery. Although the main scavenger receptor megalin remained unaltered, a new phosphorylation site at S4577 was found. The identification of the role of this mTORC1-induced ph