glucuronosyltransferase

(redirected from Glucuronyltransferase)

glu·cu·ron·o·syl·trans·fer·ase

(glū'kū-ron'ō-sil-trans'fĕr-ās),
Any of a family of enzymes that transfer d-glucuronate to the acceptor named, forming glucuronosides, for example, UDPglucuronate-bilirubin glucuronosyltransferase.
Farlex Partner Medical Dictionary © Farlex 2012
References in periodicals archive ?
GlcATI is a glucuronyltransferase involved in the biosynthesis of GAG-protein linkers for proteoglycans.
After oral administration, besides oxidative metabolism, EE undergoes glucuronidation and sulphatation by specific enzymes (e.g., glucuronyltransferase and sulphotransferase).
Willer et al., "Xylosyl- and glucuronyltransferase functions of LARGE in a-dystroglycan modification are conserved in LARGE2," Glycobiology, vol.
To prevent unconjugated bilirubin being deposited in tissues it is bound to albumin (a protein) and then transported in the blood to the liver where it is converted to its conjugated form by an enzyme called glucuronyltransferase (England, 2010; McIntosh and Stenson, 2008).
[4] Nonstandard abbreviations: MDMA, 3,4-methylenedioxymethamphetamine; DHMA, 3,4-dihydroxymethamphetamine; HMMA, 4-hydroxy-3-methoxymethamphetamine; UGT, uridine diphosphate glucuronyltransferase; MDA, 3,4-methylenedioxyamphetamine; DHA, 3,4-dihydroxyamphetamine; HMA, 4-hydroxy-3-methoxyamphetamine; pholedrine, 4-hydroxymethamphetamine; NIDA, National Institute on Drug Abuse; LC-HRMS, liquid chromatography/high-resolution mass spectrometry; GC-NICI-MS, gas chromatography/negative-ion chemical ionization mass spectrometry; [C.sub.max], maximum concentration; [C.sub.max100], [C.sub.max] normalized to 100 mg/dL creatinine; [t.sub.max], time of maximum concentration; [t.sub.onset], time of first detection; [t.sub.last detection], time of last detection.
A stepwise addition of D-glucuronic acid from UDP-D-glucuronic acid to bilirubin, takes place with the help of the enzyme UDP-glucuronate-bilirubin glucuronyltransferase. The addition of glucuronide makes conjugated bilirubin water soluble and capable of canalicular transport into the bile.
This entry of bilirubin into liver cells is enabled by an enzyme called glucuronyltransferase.
Although how TCS disrupts thyroid hormones is still unclear, our findings are biologically plausible based on evidence from animal studies concluding that TCS had the potential to influence thyroid function by changing the activity of glucuronyltransferase in Phase II (the reaction of conjugations) in the liver (Schuur et al.
Gilbert syndrome is an inborn error of bilirubin conjugation caused by mutations in the conjugating enzyme uridine diphosphate glucuronyltransferase (UGT1A1) (1).
DLCs, including some PCB congeners, bind to the aryl hydrocarbon receptor (AhR) and activate the hepatic uridine diphosphate glucuronyltransferase (UDP-GT) enzymes responsible for [T.sub.4] glucuronidation, resulting in [T.sub.4] excretion in bile.
Anti-microsomal antibodies targeting P450IA2 and P450IIIAl isoenzymes have also been reported in idiosyncratic liver injuries associated with dihydralazine and aromatic anticonvulsants, as well as anti-LKM3 antibodies directed against uridine diphosphate glucuronyltransferase (UDPGT) enzymes [24-26].
They concluded that fetal [T.sub.4] levels were affected by both reduced transplacental delivery of [T.sub.4] and increased [T.sub.4] metabolism by the induced glucuronyltransferase enzymes.