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1 ure and fatal metabolic liver disease due to fumarylacetoacetate dehydrolase (Fah) deficiency, hiHeps
2 , which converts maleylacetoacetate (MAA) to fumarylacetoacetate (FAA).
3 tary tyrosinemia type 1 have a deficiency of fumarylacetoacetate hydrolase (FAH) and develop progress
4  tyrosine catabolism caused by deficiency of fumarylacetoacetate hydrolase (FAH) and homogentisic aci
5                                              Fumarylacetoacetate hydrolase (FAH) catalyzes the hydrol
6 More than 100 mutations in the gene encoding fumarylacetoacetate hydrolase (FAH) cause hereditary tyr
7 ss of the remaining Hgd allele protects from fumarylacetoacetate hydrolase (Fah) deficiency, a geneti
8 es (BMHs) can cure the genetic liver disease fumarylacetoacetate hydrolase (Fah) deficiency.
9                         Transplantation into fumarylacetoacetate hydrolase (Fah) deficient mice was u
10              Mice doubly mutant for MAAI and fumarylacetoacetate hydrolase (FAH) died rapidly on a no
11                                              Fumarylacetoacetate hydrolase (FAH) domain-containing pr
12 tic genotoxicity in vivo, we transferred the fumarylacetoacetate hydrolase (FAH) gene by LV vectors i
13                               We deleted the fumarylacetoacetate hydrolase (Fah) gene in MISTRG mice
14 associated with point mutations in the human fumarylacetoacetate hydrolase (FAH) gene that disrupt ty
15                                              Fumarylacetoacetate hydrolase (FAH) is the last enzyme i
16 tis B virus X (HBx) gene, into the livers of fumarylacetoacetate hydrolase (Fah) mutant mice via hydr
17  analysis identified 4-OD as a member of the fumarylacetoacetate hydrolase (FAH) superfamily and impl
18 l vector targeting the expression of a human fumarylacetoacetate hydrolase (FAH) transgene in the por
19 he liver by knocking down an essential gene, fumarylacetoacetate hydrolase (Fah), and delivering an u
20 leading humanized liver mouse model in which Fumarylacetoacetate Hydrolase (Fah), Recombination Activ
21 essive liver disease caused by deficiency of fumarylacetoacetate hydrolase (FAH), to determine whethe
22 stem, we generated severely immunodeficient, fumarylacetoacetate hydrolase (Fah)-deficient mice.
23 tment partially restored splicing, generated fumarylacetoacetate hydrolase (FAH)-positive hepatocytes
24 inemia and show that the treatment generated fumarylacetoacetate hydrolase (Fah)-positive hepatocytes
25  and is caused by a deficiency in the enzyme fumarylacetoacetate hydrolase (FAH).
26 ns affecting the last enzyme in the pathway, fumarylacetoacetate hydrolase (FAH).
27 cells into syngeneic recipients deficient in fumarylacetoacetate hydrolase and manifesting tyrosinemi
28 the chemistries of ureidoglycolate lyase and fumarylacetoacetate hydrolase catalysis.
29 ocytes can repopulate the liver of mice with fumarylacetoacetate hydrolase deficiency and correct the
30 serial transplantation of hepatocytes in the fumarylacetoacetate hydrolase deficiency murine model of
31 s needed for liver regeneration in mice with fumarylacetoacetate hydrolase deficiency.
32       In this study, we investigated whether fumarylacetoacetate hydrolase deficient (FAH(-/-)) pigs,
33                                   In healthy fumarylacetoacetate hydrolase deficient mice (Fah(-/-)),
34 e exhibits a high level of similarity to the fumarylacetoacetate hydrolase family of proteins.
35 osinaemia type I, mice with mutations in the fumarylacetoacetate hydrolase gene (Fah-/-) regain norma
36                            Here, we used the fumarylacetoacetate hydrolase knockout mouse to determin
37 aperitoneal injection into 8- to 12-week-old fumarylacetoacetate hydrolase mice (Fah(-/-)), a model o
38 toring the normal functions of liver enzymes fumarylacetoacetate hydrolase or alpha-1 antitrypsin.
39 omic sequence for repairing the mutated Fah (fumarylacetoacetate hydrolase) gene.
40 al recessive disease caused by deficiency in fumarylacetoacetate hydrolase, the last enzyme in the ty
41 ion of human hepatocytes in immunodeficient, fumarylacetoacetate hydrolase-deficient (fah(-/-)) mice.
42 d libraries were delivered to hepatocytes in fumarylacetoacetate hydrolase-deficient mice at the time
43                       In addition, 28 of the fumarylacetoacetate hydrolase-deficient mice were transp
44  mice long after death and transplanted into fumarylacetoacetate hydrolase-deficient mice, a model fo
45  repopulation after toxic liver injury using fumarylacetoacetate hydrolase-deficient mice.
46 oved liver function and a better survival of fumarylacetoacetate hydrolase-deficient mice.
47 iparum LS in vivo: the immunocompromised and fumarylacetoacetate hydrolase-deficient mouse (Fah-/-, R
48 PE-corrected CdHs repopulated the liver with fumarylacetoacetate hydrolase-positive cells and dramati
49 yrosinemia type 1 is caused by deficiency of fumarylacetoacetate hydrolase.
50 ocytes expressing dipeptidyl peptidase IV or fumarylacetoacetate hydrolase.
51 trans isomerisation of maleylacetoacetate to fumarylacetoacetate is the penultimate step in the tyros
52 e enzymatic defect impairs the conversion of fumarylacetoacetate to fumarate, causing accumulation of
53 drolytic cleavage of a carbon-carbon bond in fumarylacetoacetate to yield fumarate and acetoacetate a