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