ライフサイエンスコーパス: fumarylacetoacetate hydrolase

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1 ocytes expressing dipeptidyl peptidase IV or fumarylacetoacetate hydrolase.

2 yrosinemia type 1 is caused by deficiency of 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 In addition, 28 of the fumarylacetoacetate hydrolase-deficient mice were transp

12 mice long after death and transplanted into fumarylacetoacetate hydrolase-deficient mice, a model fo

13 iparum LS in vivo: the immunocompromised and fumarylacetoacetate hydrolase-deficient mouse (Fah-/-, R

14 tary tyrosinemia type 1 have a deficiency of fumarylacetoacetate hydrolase (FAH) and develop progress

15 tyrosine catabolism caused by deficiency of fumarylacetoacetate hydrolase (FAH) and homogentisic aci

16 Fumarylacetoacetate hydrolase (FAH) catalyzes the hydrol

17 ss of the remaining Hgd allele protects from fumarylacetoacetate hydrolase (Fah) deficiency, a geneti

18 es (BMHs) can cure the genetic liver disease fumarylacetoacetate hydrolase (Fah) deficiency.

19 Transplantation into fumarylacetoacetate hydrolase (Fah) deficient mice was u

20 Mice doubly mutant for MAAI and fumarylacetoacetate hydrolase (FAH) died rapidly on a no

21 Fumarylacetoacetate hydrolase (FAH) domain-containing pr

22 tic genotoxicity in vivo, we transferred the fumarylacetoacetate hydrolase (FAH) gene by LV vectors i

23 associated with point mutations in the human fumarylacetoacetate hydrolase (FAH) gene that disrupt ty

24 tis B virus X (HBx) gene, into the livers of fumarylacetoacetate hydrolase (Fah) mutant mice via hydr

25 analysis identified 4-OD as a member of the fumarylacetoacetate hydrolase (FAH) superfamily and impl

26 essive liver disease caused by deficiency of fumarylacetoacetate hydrolase (FAH), to determine whethe

27 stem, we generated severely immunodeficient, fumarylacetoacetate hydrolase (Fah)-deficient mice.

28 inemia and show that the treatment generated fumarylacetoacetate hydrolase (Fah)-positive hepatocytes

29 ns affecting the last enzyme in the pathway, fumarylacetoacetate hydrolase (FAH).

30 and is caused by a deficiency in the enzyme fumarylacetoacetate hydrolase (FAH).

31 e exhibits a high level of similarity to the fumarylacetoacetate hydrolase family of proteins.

32 osinaemia type I, mice with mutations in the fumarylacetoacetate hydrolase gene (Fah-/-) regain norma

33 omic sequence for repairing the mutated Fah (fumarylacetoacetate hydrolase) gene.

34 Here, we used the fumarylacetoacetate hydrolase knockout mouse to determin

35 aperitoneal injection into 8- to 12-week-old fumarylacetoacetate hydrolase mice (Fah(-/-)), a model o

36 al recessive disease caused by deficiency in fumarylacetoacetate hydrolase, the last enzyme in the ty

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