Anti-ULK3 Antibody

ULK3 belongs to the Ser/Thr protein kinase superfamily and plays a role in the ATP-dependent phosphorylation of target proteins (1) . Knockout of ULK genes results in a severe defect in the autophagy pathway (2) . ULK3, like the other Unc-51-like kinases such as ULK1, ULK2 and ULK4, is highly conserved among eukaryotes (3) . ULK3 has been shown to be a positive regulator of the Hedgehog signaling pathway by enhancing GLI1 and GLI2 transcriptional activity (4) . Furthermore, ULK3 can also interact with SUFU, a protein required for the negative regulation of GLI proteins; this interaction blocks the autophosphorylation of ULK3 and blocks its ability to regulate the GLI proteins (5) .

Widely expressed. Highest levels observed in fetal brain. In adult tissues, high levels in brain, liver and kidney, moderate levels in testis and adrenal gland and low levels in heart, lung, stomach, thymus, prostate and placenta. In the brain, highest expression in the hippocampus, high levels also detected in the cerebellum, olfactory bulb and optic nerve. In the central nervous system, lowest levels in the spinal cord.

Serine/threonine protein kinase that acts as a regulator of Sonic hedgehog (SHH) signaling and autophagy. Acts as a negative regulator of SHH signaling in the absence of SHH ligand: interacts with SUFU, thereby inactivating the protein kinase activity and preventing phosphorylation of GLI proteins (GLI1, GLI2 and/or GLI3) . Positively regulates SHH signaling in the presence of SHH: dissociates from SUFU, autophosphorylates and mediates phosphorylation of GLI2, activating it and promoting its nuclear translocation. Phosphorylates in vitro GLI2, as well as GLI1 and GLI3, although less efficiently. Also acts as a regulator of autophagy: following cellular senescence, able to induce autophagy.