High impact information on Ugt1a6a

• Cloning and characterization of cDNAs encoding mouse Ugt1.6 and rabbit UGT1.6: differential induction by 2,3,7,8-tetrachlorodibenzo-p-dioxin [1].
• To examine the substrate specificities of the proteins encoded by the mouse Ugt1.6 and rabbit UGT1.6 cDNAs, the recombinants were expressed in monkey kidney COS-1 cells [1].
• Transfection of the mouse and rabbit recombinants allowed for the expression of the UGT1.6 proteins as determined by immunoprecipitation of newly synthesized protein [1].
• Likewise, V79 cells transfected with the 3-MC-inducible rat UGT1.6 cDNA showed a considerable rate of PH and HQ glucuronidation [2].
• The effect of malaria infection on UDP-glucuronosyltransferase (UDPGT) activity was investigated in rat liver microsomes using 3'-azido-3'-deoxythymidine and paracetamol [3].

Biological context of Ugt1a6a

• Two genes are members of the [Ah] battery and induced by ROM-mediated oxidative stress: NAD(P)H:menadione oxidoreductase (Nmo1) and UDP glucuronosyltransferase-1A6 (Ugt1a6) [4].
• Isolation of cDNAs for mouse phenol and bilirubin UDP-glucuronosyltransferases and mapping of the mouse gene for phenol UDP-glucuronosyltransferase (Ugtla1) to chromosome 1 by restriction fragment length variations [5].
• Based on sequence homology and common catalytic activity, this dog UGT1A protein appears to be the canine orthologue of human UGT1A6 [6].
• The UGT1A6 P1 promoter lacks an HNF1 binding site in the analogous position and showed little response to HNF1 overexpression [7].

Anatomical context of Ugt1a6a

• The activities of EROD, MROD, PROD, PNPH, GST, UDPGT and NQO1 were measured in the liver and kidney microsomes of female Swiss mice treated intraperitoneally (i.p.) with protocatechuic acid in the dose range of 80-800 mg/kg [8].

Associations of Ugt1a6a with chemical compounds

• We also detected duplication of the gene for phenol UDPGT in all mouse strains examined with the exception of MOL-MIT and SUB-SHH [5].
• The enzyme expressed stably in V79 cells predominantly catalyzed the glucuronidation of simple, planar phenols (e.g., for 1-naphthol, K(m) = 41 microM, V(max) = 0.07 nmol/min/mg protein), a class of compounds extensively glucuronidated by human UGT1A6 [6].
• Induction of UGT1A6 is thought to be responsible at least partly for reduced serum thyroid hormone levels in TCDD-exposed mice [9].

Other interactions of Ugt1a6a

• In liver plus nine extrahepatic tissues of untreated newborn 14CoS/14CoS mutant and ch/ch wild-type mice, we compared NMO1, UGT1A6, AHD3 and HNF-1 alpha mRNA levels [4].
• Male-predominant expression was observed for Ugt2b1 in liver, Ugt2b5/37/38 in kidney, and Ugt1a6 in lung [10].
• PhSCA also increased GstP, and PhOHSCA increased Ugt1a1 and Ugt1a6 levels [11].
• P-450 content and the UDPGT activity were significantly elevated (p < 0.01-0.001) from the early stages of tumor growth while the cytosolic GSHT activity reached its highest level (p < 0.01-0.001) only 10 days after tumor transplantation [12].

Analytical, diagnostic and therapeutic context of Ugt1a6a

• However, when New Zealand white rabbits were treated with TCDD and liver mRNA was examined by Northern blot analysis, it was shown that TCDD had no effect on the induction of UGT1.6 mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)[1]

References