Target intelligence / Profile preview

Carbohydrate sulfotransferase 5 (CHST5)

Target
CHST5
Molecular classification
Enzyme, Sulfotransferase, Type II membrane protein
01

Overview

Carbohydrate sulfotransferase 5 (CHST5) is a type II Golgi-localized membrane enzyme that transfers a sulfate group from the donor molecule 3'-phospho-5'-adenylyl sulfate (PAPS) to the 6-O position of galactose, N-acetylgalactosamine, or N-acetylglucosamine residues on proteoglycans and glycoproteins[1][2][4][6]. This sulfation reaction modifies the structural properties of mucins and other carbohydrates, which can affect their recognition by extracellular matrix proteins, receptors, and viruses and influence biological processes such as cell-cell communication, mucosal barrier function, and immune modulation[2]. CHST5 is predominantly expressed in intestinal tissues such as the colon and small intestine[1][2][6]. Its altered expression and function have been studied in the context of neurodegenerative diseases (notably Alzheimer's disease) and gastrointestinal tract physiology, but there are no approved drugs targeting CHST5 nor definitive clinical safety concerns currently reported[1][6].

Other names
I-GlcNAc-6-STI-GlcNAc6STglcNAc6ST-3gn6st-3hIGn6STGlcNAc6ST-3GST4-alphaN-acetylglucosamine 6-O-sulfotransferase 3intestinal GlcNAc-6-sulfotransferaseFLJ22167galactose/N-acetylglucosamine/N-acetylglucosamine 6-O-sulfotransferase 4-alpha
02

Biological functions

Carbohydrate sulfationTransfer of sulfate to position 6 of galactose (Gal), N-acetylgalactosamine (GalNAc), and N-acetylglucosamine (GlcNAc) residuesModification of proteoglycans and glycoproteinsCreation of specific extracellular matrix epitopesMucin-type O-linked sugar modification[1][2][4][6]
03

Disease associations

Other (altered expression and association may be involved in some diseases such as neurodegenerative disorders, specifically noted in Alzheimer’s disease risk and pathology studies, but not a primary reported cancer gene)[1]
04

Biomarkers

Glycodeoxycholate (noted as associated metabolite in AD genetic mapping studies)[1]

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