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3.2.1.31
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Showing 1-11 of 11 results for "3.2.1.31 " within Papers
J W Kyle et al.
Proceedings of the National Academy of Sciences of the United States of America, 87(10), 3914-3918 (1990-05-01)
We recently described a murine model for mucopolysaccharidosis VII in mice that have an inherited deficiency of beta-glucuronidase (beta-D-glucuronoside glucuronosohydrolase, EC 3.2.1.31). Affected mice, of genotype gusmps/gusmps, present clinical manifestations similar to those of humans with mucopolysaccharidosis VII (Sly syndrome)
M T Watts et al.
Journal of chromatography, 230(1), 79-86 (1982-06-11)
We have developed a rapid, sensitive and precise high-performance liquid chromatographic method using fluorescence detection for the simultaneous determination of thiabendazole and unconjugated 5-hydroxythiabendazole in serum. Sample pretreatment consists only of protein precipitation with acetonitrile containing the internal standard, 2-methylindole.
A Oshima et al.
Proceedings of the National Academy of Sciences of the United States of America, 84(3), 685-689 (1987-02-01)
We report here the cDNA sequence for human placental beta-glucuronidase (beta-D-glucuronoside glucuronosohydrolase, EC 3.2.1.31) and demonstrate expression of the human enzyme in transfected COS cells. We also sequenced a partial cDNA clone from human fibroblasts that contained a 153-base-pair deletion
Y C Ho et al.
Enzyme, 33(1), 9-17 (1985-01-01)
beta-Glucuronidase (EC 3.2.1.31) was purified from human liver and its activity was determined by enzyme kinetic method employing phenolphthalein glucuronic acid (PGA) and conjugated bilirubin, primarily bilirubin diglucuronide purified from human bile, as substrates in the absence or presence of
R Palmer et al.
Proceedings of the National Academy of Sciences of the United States of America, 80(24), 7596-7600 (1983-12-01)
A cis-acting genetic element, designated Gus-r, regulates the androgen-induced rates of murine glucuronidase (EC 3.2.1.31) synthesis in kidney tubule cells and is tightly linked to the glucuronidase structural gene, Gus-s. To investigate the molecular mechanism underlying this regulation, we have
A Fujinami et al.
Biological & pharmaceutical bulletin, 21(11), 1207-1210 (1998-12-16)
We developed a method for simultaneous analysis of benzphetamine (BZ) and its metabolites, p-hydroxy-N-benzylamphetamine (pHBA), p-hydroxybenzphetamine (pHBZ), amphetamine (AP), methamphetamine and p-hydroxymethamphetamine by micellar electrokinetic chromatography (MEKC). Urine samples from 0-15 h (3-h intervals) after oral administration of BZ (10
S L Naylor et al.
Proceedings of the National Academy of Sciences of the United States of America, 75(12), 6159-6162 (1978-12-01)
Argininosuccinic aciduria, an autosomal recessive disorder of the urea cycle in humans, is associated with a deficiency of argininosuccinate lyase (ASL; L-argininosuccinate arginine-lyase, EC 4.3.2.1). ASL activity was visualized on gels after electrophoresis by a new method, termed bioautography. Bioautography
Loganathan Arul et al.
Bioinformation, 2(8), 339-343 (2008-08-08)
Glycosyl hydrolases hydrolyze the glycosidic bond either in carbohydrates or between carbohydrate and non-carbohydrate moiety. The beta-glucuronidase (beta D-glucuronoside glucuronosohydrolase; EC 3.2.1.31) enzyme belongs to the family-2 glycosyl hydrolase. The E. coli borne beta-glucuronidase gene (uidA) was devised as a
S W Toennes et al.
Clinical chemistry, 45(12), 2173-2182 (1999-12-10)
Cleavage of conjugates is an important step in toxicological analysis, especially of urine samples. The aim of this study was to combine the advantages and to reduce the disadvantages of acid hydrolysis and conventional enzymatic hydrolysis procedures. beta-Glucuronidase (GRD; EC
Shunji Tomatsu et al.
Human mutation, 30(4), 511-519 (2009-02-19)
Mucopolysaccharidosis VII (MPS VII; Sly syndrome) is an autosomal recessive disorder caused by a deficiency of beta-glucuronidase (GUS, EC 3.2.1.31; GUSB). GUS is required to degrade glycosaminoglycans (GAGs), including heparan sulfate (HS), dermatan sulfate (DS), and chondroitin-4,6-sulfate (CS). Accumulation of
E M Schmelz et al.
Cancer research, 59(22), 5768-5772 (1999-12-03)
Dietary sphingolipids inhibit chemically induced colon cancer in mice. The most likely mediators of this effect are the metabolites ceramide (Cer) and sphingosine, which induce growth arrest and apoptosis in transformed cells. Sphingolipids are digested in both the upper and
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