Inducible myeloid cell leukemia 1 protein (IML1 (in yeast); in mammals, the canonical homolog is DEPDC5)

Inducible myeloid cell leukemia 1 protein (Iml1p) is a scaffold component of the Iml1-Npr2-Npr3 complex in yeast, which regulates autophagy in response to specific nutrient signals, notable for acting under non-nitrogen-starvation conditions[1]. Its function is conserved in higher eukaryotes, where the ortholog DEPDC5 forms a key part of the GATOR1 complex, a negative regulator of the mTORC1 pathway that acts as a GTPase-activating protein towards Rag GTPases, thereby inhibiting mTORC1 in conditions of amino acid starvation[2]. GATOR1/DEPDC5 participates in the regulation of cell growth, metabolism, autophagy, and the transition from mitosis to meiosis in response to the nutrient environment. While essential for nutrient sensing and metabolic homeostasis, Iml1/DEPDC5 is not a classical therapeutic target; however, its pathway is of great interest in cancer, metabolic diseases, and basic research into the mTOR signaling cascade[1][2].

Other names

Iml1pGATOR1 complex subunit Iml1 (in yeast)DEPDC5 (human ortholog)GATOR1 catalytic subunit (in mammalian systems)RANS domain-containing protein (refers to a conserved domain within the protein)GATOR complex component (in higher eukaryotes)

Not applicable (there are no clinical-stage drugs, but mechanistically, loss-of-function or knockdowns lead to hyperactivation of TORC1 signaling. Therefore, potential mechanisms could involve indirect suppression of mTOR inhibitors or upstream nutrient-sensing regulators in research settings)[2].