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1 aline phosphatase and Pseudomonas aeruginosa arylsulfatase.
2 ystallographic data for three highly related arylsulfatases.
3 hows no sequence similarity with other known arylsulfatases.
4  (LC-MS/MS) assays were developed to measure arylsulfatase A (ARSA) activity in leukocytes and dried
5 ctrophotometric method, the determination of arylsulfatase A (ARSA) activity toward the natural subst
6 vivo with a lentiviral vector encoding human arylsulfatase A (ARSA) cDNA, and compared with an untrea
7 e disorder caused mainly by mutations in the arylsulfatase A (ARSA) gene.
8 22S1743 and D22S1744, were developed for the arylsulfatase A (ARSA) region of chromosome 22q.
9  that pathogenic and protective mutations in arylsulfatase A (ARSA), a gene responsible for metachrom
10 l storage disorder caused by a deficiency of arylsulfatase A (ARSA).
11 fy small molecules that enhance the residual arylsulfatase A (ASA) activity found in patients with me
12 eural precursors (NPs) that are deficient in arylsulfatase A (ASA) activity.
13                   An inherited deficiency of arylsulfatase A (ASA) causes the lysosomal storage disea
14 omote brain delivery of the lysosomal enzyme arylsulfatase A (ASA).
15 ase II and by assaying enzyme activities for arylsulfatase A and carnitine palmitoyltransferase.
16 nization of a recombinant glycoprotein human arylsulfatase A even when their rapid interconversion pr
17  storage disorder caused by mutations in the arylsulfatase A gene (ARSA) and categorized into three s
18 Sap B) is an essential activator protein for arylsulfatase A in the hydrolysis of sulfatide, a lipid
19                                              Arylsulfatase A is an endogenous enzyme that is responsi
20 epsin A, cathepsin D, alpha-galactosidase A, arylsulfatase A, and alpha-iduronidase.
21 lipid rafts isolated from wild-type mice and arylsulfatase A-deficient (ASA knockout) mice that accum
22  of canine HSS, based on homology with human arylsulfatases A and B, suggested the pathogenic effect
23  storage disorder caused by mutations in the arylsulfatase-A gene (ARSA).
24               Co-expression of a therapeutic Arylsulfatase-A with RgE-tuned levels of the required he
25 accumulate sulfatides due to a deficiency in arylsulfatase-A, directly activate iNKT cells.
26 ers (beta-glucosidase, alkaline phosphatase, arylsulfatase activities and fluorescein diacetate hydro
27 th nutrient-replete growth and P limitation; arylsulfatase activity and S deficiency-responsive genes
28          Clinical isolates were positive for arylsulfatase activity at 3 days, nitrate, iron uptake,
29 r1sac1snrk2.2 triple mutants exhibit reduced arylsulfatase activity compared to snrk2.2 or psr1snrk2.
30                    The sac3 mutant expresses arylsulfatase activity even when grown in nutrient-reple
31                          In wild-type cells, arylsulfatase activity is detected only during sulfur li
32 demonstrate that the mammalian Sulfs exhibit arylsulfatase activity with a pH optimum in the neutral
33                 In contrast to its effect on arylsulfatase activity, Sac3 positively regulates the hi
34 ntial for endosulfatase activity but not for arylsulfatase activity.
35 in has a negative effect on the induction of arylsulfatase activity.
36  specific enzymes (1, 4-beta-cellobiosidase, arylsulfatase, alkaline phosphatase, and phenol oxidase)
37 d a new methodology utilizing an immobilized arylsulfatase and an immobilized beta-glucuronidase to m
38 and consequently these cells synthesize some arylsulfatase and exhibit elevated levels of transcripts
39 xemplified by the synthesis of extracellular arylsulfatase and the accumulation of transcripts encodi
40 lagellation responsiveness to a promoterless arylsulfatase (ARS) gene.
41 ferred partial acid shock inducibility to an arylsulfatase (ARS) reporter gene.
42 iggered accumulation of transcripts encoding arylsulfatases (ARS), an extracellular polypeptide that
43 nes that encode nitrate reductase (NITI) and arylsulfatase (ARS2) transcriptionally fused to sequence
44 tein (Rasa), dihydrofolate reductase (Dhfr), arylsulfatase (As-1), thrombin receptor (Cf2r), hexosami
45  maps out the likely transition zone between arylsulfatases (ASs) and phosphonate monoester hydrolase
46 sents evidence that deficiency of the enzyme arylsulfatase B (ARSB; N-acetylgalactosamine 4-sulfatase
47 n, and decline in the activity of the enzyme arylsulfatase B (ARSB; N-acetylgalactosamine-4-sulfatase
48 wed that treatment by recombinant human (rh) Arylsulfatase B (ARSB; N-acetylgalactosamine-4-sulfatase
49  enzymes, N-acetylgalactosamine-4-sulfatase (arylsulfatase B (ASB)) and galactose-6-sulfatase (GALNS)
50 disorder caused by the deficient activity of arylsulfatase B (ASB).
51 disorder caused by the deficient activity of arylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase)
52                                              Arylsulfatase B (N-acetylgalactosamine-4-sulfatase; ARSB
53  intracellular activity of recombinant human arylsulfatase B (rhASB) on its natural glycosaminoglycan
54  colonic epithelial cells through decline in arylsulfatase B activity, with subsequent impact on C4S,
55      Reducing 4S with the 4-sulfatase enzyme Arylsulfatase-B (ARSB) enhanced outgrowth of dissociated
56 by loss of function of the steroid sulfatase arylsulfatase C (STS), to develop a model of corrective
57                   For Pseudomonas aeruginosa arylsulfatase-catalyzed aryl sulfate hydrolysis, Bronste
58 s to sulfur limitation; it cannot synthesize arylsulfatase, does not take up sulfate as rapidly as wi
59 ibrary for HYDA1 promoter activity using the arylsulfatase-encoding ARYLSULFATASE2 gene as a selectio
60            We also evaluated the efficacy of arylsulfatase enzymatic activity as a reporter and found
61 oding cluster and a region encoding putative arylsulfatase enzymes, which were conserved across geogr
62 sigmas, including SigW-1, which orchestrates arylsulfatase expression critical for host colonization,
63                       One of these proteins, arylsulfatase F (ARSF), was studied by immunofluorescenc
64 oduct shows homology to a well-characterized arylsulfatase family of enzymes found in eukaryotes, as
65                                              Arylsulfatase G (ARSG) is a recently identified lysosoma
66              Here we show that the lysosomal arylsulfatase G (ARSG) is the long-sought glucosamine-3-
67                                Deficiency of arylsulfatase G (ARSG) leads to a lysosomal storage dise
68                                          The arylsulfatase gene from Campylobacter jejuni 81-176 enco
69 notypes, the cheY gene was inserted into the arylsulfatase gene of 81-176 to generate a strain with t
70 ere we report the functional analysis of the arylsulfatase insulator (ArsI) derived from the sea urch
71               A novel member of this family, arylsulfatase K (ARSK), was identified bioinformatically
72  for microorganism identification or exhibit arylsulfatase, lactonase, or phosphotriesterase activiti
73 on in vivo, we identified six genes encoding arylsulfatase-like enzymes with a predicted C-terminal t
74 mined to be homologous to E. coli K-12 aslA (arylsulfatase-like gene).
75 fication; of note, N. nova were positive for arylsulfatase, N. farcinica were positive for opacificat
76  of two YejM homologues with hydrolases like arylsulfatases, no enzymatic activity has been previousl
77 mains of PbgA resemble the structures of the arylsulfatase protein family and contains a novel core h
78           The ars76 mutant cannot accumulate arylsulfatase protein or mRNA and shows marked alteratio
79 Tween 80 hydrolysis, tellurite reduction, or arylsulfatase reduction; grew best at low salt concentra
80                                              Arylsulfatases require a maturating enzyme to perform a
81 tic analysis of coleopteran and lepidopteran arylsulfatases, the P. chrysocephala GSSs formed a clust
82 3)CR1-expressing cell membranes treated with arylsulfatase to desulfate tyrosine residues also showed
83 activity upon phosphorus deprivation and the arylsulfatase upon sulfur deprivation, suggesting that t
84 e as a cofactor in a class of enzymes termed arylsulfatases, which catalyze the hydrolysis of various
85 ystal structure shows structural homology to arylsulfatases with conservation of the core alpha/beta-