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Hexosaminidase

Hexosaminidase is an enzyme involved in the hydrolysis of terminal N-acetyl-D-hexosamine residues in N-acetyl-β-D-hexosaminides.

Isoenzymes and genes
Lysosomal A, B, and S isoenzymes Functional lysosomal β-hexosaminidase enzymes are dimeric in structure. Three isoenzymes are produced through the combination of α and β subunits to form any one of three active dimers: The α and β subunits are encoded by separate genes, HEXA and HEXB respectively. β-Hexosaminidase and the cofactor GM2 activator protein catalyze the degradation of the GM2 gangliosides and other molecules containing terminal N-acetyl hexosamines. Gene mutations in HEXB often result in Sandhoff disease; whereas, mutations in HEXA decrease the hydrolysis of GM2 gangliosides, which is the main cause of Tay–Sachs disease. Function Even though the α and β subunits of lysosomal hexosaminidase can both cleave GalNAc residues, only the α subunit is able to hydrolyze GM2 gangliosides because of a key residue, Arg-424, and a loop structure that forms from the amino acid sequence in the alpha subunit. The loop in the α subunit, consisting of Gly-280, Ser-281, Glu-282, and Pro-283 which is absent in the β subunit, serves as an ideal structure for the binding of the GM2 activator protein (GM2AP), and arginine is essential for binding the N-acetyl-neuraminic acid residue of GM2 gangliosides. The GM2 activator protein transports GM2 gangliosides and presents the lipids to hexosaminidase, so a functional hexosaminidase enzyme is able to hydrolyze GM2 gangliosides into GM3 gangliosides by removing the N-acetylgalactosamine (GalNAc) residue from GM2 gangliosides. The most common mutation, which occurs in over 80 percent of Tay–Sachs patients, results from a four base pair addition (TATC) in exon 11 of the Hex A gene. This insertion leads to an early stop codon, which causes the Hex A deficiency. Children born with Tay–Sachs usually die between two and four years of age from aspiration and pneumonia. Tay–Sachs causes cerebral degeneration and blindness. Patients also experience flaccid extremities and seizures. At present there has been no cure or effective treatment of Tay–Sachs disease. The two subunits of hexosaminidase A are shown below: Cytosolic C and D isozymes The bifunctional protein NCOAT (nuclear cytoplasmic O-GlcNAcase and acetyltransferase) that is encoded by the MGEA5 gene possesses both hexosaminidase and histone acetyltransferase activities. NCOAT is also known as hexosaminidase C and has distinct substrate specificities compared to lysosomal hexosaminidase A. A single-nucleotide polymorphism in the human O-GlcNAcase gene is linked to diabetes mellitus type 2. A fourth mammalian hexosaminidase polypeptide which has been designated hexosaminidase D (HEXDC) has recently been identified. == References ==
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