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, Ser27-Asn395, with an N-terminal 6-His tag Accession #:NP_067628 N-terminal Sequence Analysis:His Purity:>95%, by SDS-PAGE under reducing conditions and visualized by silver stain. Endotoxin Level: Predicted Molecular Mass:42 kDa SDS-PAGE:55 kDa, under reducing conditions Activity:Measured by its ability to transfer sulfate from PAPS to N-acetyl-D-glucosamine.The specific activity is >50 pmol/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: Carbohydrate Sulfotransferase 6/CHST6 Aliases: C-GlcNAc6ST; CGn6ST; CHST6; GlcNAc6ST-5; GST4-beta; MCDC1 Entrez Gene IDs: 4166 (Human); 56773 (Mouse); 307859 (Rat) Background: Carbohydrate Sulfotransferase 6 The CHST family is comprised of 14 genes in humans. All members of this family are Golgi-localized type II membrane proteins. Only the luminal and enzymatic domain is expressed in each of R&D Systems recombinant CHST proteins. These enzymes transfer sulfate (i.e., sulfonate) onto the 6-O or 4-O positions of GalNAc, Gal and GlcNAc residues on glycoproteins, proteoglycans and glycolipids. This sulfation often creates specific epitopes that can be recognized by extracellular matrix proteins, cell surface receptors and viruses. CHST6, also designated as corneal N-acetylglucosamine-6-O-sulfotransferase or N-acetylglucosamine 6-O-sulfotransferase 5, transfers sulfate to position 6 of non-reducing GlcNAc residues of keratan sulfate found in the corneal stroma. It also acts on the non-reducing terminal GlcNAc residues of carbohydrate substrates that have poly-N-acetyllactosamine structures. Defects in CHST6 cause macular corneal dystrophy, an autosomal recessive disease characterized by corneal opacities.