The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Protein concentration is above or equal to 0.05 mg/ml.
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Preparation and Storage
Stability and Storage
Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
pH: 8.00 Constituents: 0.31% Glutathione, 0.79% Tris HCl
Bilirubin UDP glucuronosyltransferase isozyme 2
Bilirubin-specific UDPGT isozyme 2
UDP glucuronosyltransferase 1 family polypeptide A4
UDP glycosyltransferase 1 family polypeptide A4
UDPGT is of major importance in the conjugation and subsequent elimination of potentially toxic xenobiotics and endogenous compounds. This isoform glucuronidates bilirubin IX-alpha to form both the IX-alpha-C8 and IX-alpha-C12 monoconjugates and diconjugate.
Expressed in liver. Not expressed in skin or kidney.
Involvement in disease
Defects in UGT1A4 are the cause of Gilbert syndrome (GILBS) [MIM:143500]. Gilbert syndrome occurs as a consequence of reduced bilirubin transferase activity and is often detected in young adults with vague nonspecific complaints. Defects in UGT1A4 are the cause of Crigler-Najjar syndrome type 1 (CN1) [MIM:218800]. CN1 patients have severe hyperbilirubinemia and usually die of kernicterus (bilirubin accumulation in the basal ganglia and brainstem nuclei) within the first year of life. CN1 inheritance is autosomal recessive. Defects in UGT1A4 are the cause of Crigler-Najjar syndrome type 2 (CN2) [MIM:606785]. CN2 patients have less severe hyperbilirubinemia and usually survive into adulthood without neurologic damage. Phenobarbital, which induces the partially deficient glucuronyl transferase, can diminish the jaundice. CN2 inheritance is autosomal dominant.