金山科研平台，产品价格货期咨询微信：jinshanbio Source:Chinese Hamster Ovary cell line, CHO-derived, Gly17-Val525, with a C-terminal 10-His tag Accession #:Q3TYD4 N-terminal Sequence Analysis:Gly17 Purity:>95%, by SDS-PAGE under reducing conditions and visualized by silver stain. Endotoxin Level: Predicted Molecular Mass:57 kDa SDS-PAGE:65 kDa, reducing conditions Activity:Measured by its ability to hydrolyze the substrate 4-Nitrocatechol Sulfate (PNCS). The specific activity is >1,500pmol/min/µg, as measured under the described conditions. Formulation:Supplied as a 0.2 µm filtered solution in Tris and NaCl.See Certificate of Analysis for details. Molecule Information: Arylsulfatase G/ARSG Aliases: ARSG; ASG Entrez Gene IDs: 22901 (Human); 74008 (Mouse); 303631 (Rat) Background: Sulfatases Sulfatases belong to a highly conserved family of enzymes that catalyze the hydrolysis of O- and N-sulfate esters from a variety of substrates. Among 18 human sulfatase genes identified, about 1/3 are found in lysosomes and serve to remove sulfate from glycosaminoglycans (GAGs), glycopeptides and glycolipids (GLs). The remaining sulfatases are found in microsomes, endoplasmic reticulum (ER), Golgi, at the cell surface, or secreted and are active against hydroxysteroids, heparin or unidentified substrates. Genetic deficiencies of individual sulfatases reveal the critical importance of these enzymes in the metabolism of specific forms of sulfate. Deficiencies of lysosomal sulfatases that act on GAGs and GLs account for mucopolysaccharidoses (MPS) and metachromatic leukodystrophy, respectively. Deficiencies in non-lysosomal sulfatases, arylsulfases C and E, cause X-linked ichthyosis (XLI) and chondrodysplasia punctata (CDPX), respectively.