Predicted to enable UDP-glycosyltransferase activity and protein dimerization activity. Predicted to contribute to glucuronosyl-N-acetylglucosaminyl-proteoglycan 4-alpha-N-acetylglucosaminyltransferase activity. Predicted to be involved in glycosaminoglycan biosynthetic process; heparan sulfate proteoglycan biosynthetic process, polysaccharide chain biosynthetic process; and ossification. Predicted to act upstream of or within with a positive effect on several processes, including cell surface receptor signaling pathway; embryonic morphogenesis; and podocyte differentiation. Predicted to act upstream of or within several processes, including cell surface receptor signaling pathway; extracellular matrix organization; and skeletal system development. Predicted to be located in endoplasmic reticulum membrane. Predicted to be part of catalytic complex. Predicted to be active in Golgi apparatus. Human ortholog(s) of this gene implicated in chondrosarcoma and hereditary multiple exostoses. Orthologous to human EXT1 (exostosin glycosyltransferase 1); PARTICIPATES IN heparan sulfate biosynthetic pathway; INTERACTS WITH 6-propyl-2-thiouracil; amitrole; bisphenol A.
[[Gasoline co-treated with 1-Butanol] results in increased abundance of [Particulate Matter co-treated with Polycyclic Aromatic Hydrocarbons]] which results in increased expression of EXT1 mRNA
[NOG protein co-treated with Panobinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of EXT1 mRNA
[NOG protein co-treated with trichostatin A co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of EXT1 mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in decreased expression of EXT1 mRNA
Expression of Ext1, Ext2, and heparanase genes in brain of senescence-accelerated OXYS rats in early ontogenesis and during development of neurodegenerative changes.