SCUBA

ULK1 — Unc-51 like autophagy activating kinase 1

ULK1 belongs to a gene co-expression module in 1 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

ULK1's module in each cell type

Cell typeModuleShares the module with
MonocytesAutophagy Initiation
Lysosomal & pahgocytosis
AAK1, AGFG1, ARID3B, FHIP2A, PHC2, PTK2B, RIOK3, TMCO3 +1 moreView in SCUBA

About the gene

SynonymsATG1, ATG1A
Chromosome12: 131894622-131923150
Predicted locationIntracellular
Essential geneNo
Protein classEnzymes, Plasma proteins, Predicted intracellular proteins
Molecular functionKinase, Serine/threonine-protein kinase, Transferase
Biological processAutophagy

Function

Serine/threonine-protein kinase involved in autophagy in response to starvation. Acts upstream of phosphatidylinositol 3-kinase PIK3C3 to regulate the formation of autophagophores, the precursors of autophagosomes. Part of regulatory feedback loops in autophagy: acts both as a downstream effector and negative regulator of mammalian target of rapamycin complex 1 (mTORC1) via interaction with RPTOR. Activated via phosphorylation by AMPK and also acts as a regulator of AMPK by mediating phosphorylation of AMPK subunits PRKAA1, PRKAB2 and PRKAG1, leading to negatively regulate AMPK activity. May phosphorylate ATG13/KIAA0652 and RPTOR; however such data need additional evidences. Plays a role early in neuronal differentiation and is required for granule cell axon formation. Also phosphorylates SESN2 and SQSTM1 to regulate autophagy. Phosphorylates FLCN, promoting autophagy. Phosphorylates AMBRA1 in response to autophagy induction, releasing AMBRA1 from the cytoskeletal docking site to induce autophagosome nucleation. Phosphorylates ATG4B, leading to inhibit autophagy by decreasing both proteolytic activation and delipidation activities of ATG4B.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.