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1 ep trefoil knot was found in acetylornithine transcarbamylase.
2 designate this enzyme as an acetylornithine transcarbamylase.
3 is protein is a novel N-succinyl-L-ornithine transcarbamylase.
4 thine transcarbamylase rather than ornithine transcarbamylase.
5 region, and the pyrB gene encoding aspartate transcarbamylase.
6 dence of the kinetic parameters of aspartate transcarbamylase.
7 sm genes and the urea cycle enzyme ornithine transcarbamylase.
8 inhibitors specific to this novel family of transcarbamylases.
9 rginine biosynthesis and on the evolution of transcarbamylases.
10 ficant domain closure take place as in other transcarbamylases.
11 pressing the liver-specific enzyme ornithine transcarbamylase administered to the lungs of various st
14 carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase (CAD), and metabolo
15 carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase (CAD), and mevalona
16 carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase (CAD), which cataly
17 D (carbamoyl-phosphate synthase 2, aspartate transcarbamylase, and dihydroorotase complex) activation
19 mpestris, the protein annotated as ornithine transcarbamylase, and encoded by the argF gene, is unabl
20 and regulation of Escherichia coli aspartate transcarbamylase, and modeling has suggested that long r
23 oyl-phosphate synthetase 2 (CPS2), aspartate transcarbamylase (ATCase) and dihydroorotase (DHOase) ac
24 nal transition of Escherichia coli aspartate transcarbamylase (ATCase) by measuring (1) hydration cha
27 ne transcarbamylases (OTCases) and aspartate transcarbamylases (ATCases); however, the second substra
28 e incorporated into 'mature' human ornithine transcarbamylase cDNA and overexpressed in Escherichia c
31 iency (0.35 +/- 0.11), and partial ornithine transcarbamylase deficiency (0.26 +/- 0.06) from normal
33 chieved significant improvement of ornithine transcarbamylase deficiency (OTCD) in a mouse model thro
36 e model of the urea cycle disorder ornithine transcarbamylase deficiency (OTCD) using patient-derived
39 models of hyperammonemia (genetic ornithine transcarbamylase deficiency and bile duct ligation-induc
40 he long-term outcome in girls with ornithine transcarbamylase deficiency enrolled in studies of treat
41 al approach achieved correction of ornithine transcarbamylase deficiency in the neonatal Spf(ash) mou
43 32 girls (age, 1 to 17 years) with ornithine transcarbamylase deficiency who had had at least one epi
45 e disease, methylmalonic aciduria, ornithine transcarbamylase deficiency, phenylketonuria, propionic
46 including acute liver failure and ornithine transcarbamylase deficiency, the most frequent urea-cycl
49 , and urea kinetics in healthy and ornithine transcarbamylase-deficient (OTCD) subjects and the possi
50 stable phenotype correction in the ornithine transcarbamylase-deficient Spf(ash) mouse and the neonat
52 n evolution and that the canonical ornithine transcarbamylase-dependent pathway became the prevalent
53 he carbamoyl-phosphate synthetase2-aspartate transcarbamylase-dihydroorotase (cad) gene as possibly c
54 Carbamoyl phosphate synthetase/aspartate transcarbamylase/dihydroorotase (CAD) is an enzyme requi
55 e carbamoyl phosphate synthetase 2/aspartate transcarbamylase/dihydroorotase multi-enzyme complex.
56 rate of CAD (carbamyl-P synthetase/aspartate transcarbamylase/dihydroorotase) gene amplification is e
59 ticle, we demonstrate that a human ornithine transcarbamylase gene containing various PTC-inducing no
60 Although many mutations in the ornithine transcarbamylase gene have been correlated with 'late on
61 d a cDNA sequence coding for human ornithine transcarbamylase in a yeast/bacterial shuttle vector, wh
62 ine transcarbamylase that replaces ornithine transcarbamylase in the canonic arginine biosynthetic pa
63 e recently reported for N-acetyl-L-ornithine transcarbamylase indicates that amino acid residue 90 (B
64 ors by treatment with the specific aspartate transcarbamylase inhibitor N-phosphonacetyl-l-aspartate
70 ulline occurs due to arginase- and ornithine transcarbamylase-mediated reactions and this limits the
72 cies of the mitochondrial enzymes, ornithine transcarbamylase (OTC) and carbamyl-phosphate synthase (
74 zed a gene coding for mature human ornithine transcarbamylase (OTC) by recursive PCR using 18 oligode
75 ions in the X-linked gene encoding ornithine transcarbamylase (OTC) cause the most common urea cycle
77 al and biochemical presentation of ornithine transcarbamylase (OTC) deficiency, we identified copy-nu
79 However, studying the efficacy of ornithine transcarbamylase (OTC) mRNA therapy in traditional knock
80 approach to improve the potency of ornithine transcarbamylase (OTC), a urea cycle enzyme for which lo
84 n in mRNA was observed in CPS1 and ornithine transcarbamylase (OTC1) in simple steatosis and NASH-fib
86 carbamylase (AOTCase), rather than ornithine transcarbamylase (OTCase), is the essential carbamylase
87 inding site is similar to those in ornithine transcarbamylases (OTCases) and aspartate transcarbamyla
88 otif that is characteristic of all ornithine transcarbamylases (OTCases) and contains a novel proline
89 plant pathogens that utilize acetylornithine transcarbamylase rather than ornithine transcarbamylase.
90 ed a synthetic gene encoding human ornithine transcarbamylase (sOTC), designed to allow mitochondrial
91 homonas campestris a novel N-acetylornithine transcarbamylase that replaces ornithine transcarbamylas
93 nts of two systems, hemoglobin and aspartate transcarbamylase, that are well described by the classic
94 ate binding occurs in N-succinyl-L-ornithine transcarbamylase, while movement of the 80 loop and sign