ライフサイエンスコーパス: FAH

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1 FAH(-/-) pigs were treated with the protective drug 2-(2

2 t the development and characterization of an FAH inhibitor, 4-(hydroxymethylphosphinoyl)-3-oxo-butano

3 ovirus injections >90% of hepatocytes became FAH positive and liver function was restored to normal.

4 her fumarylacetoacetate hydrolase deficient (FAH(-/-)) pigs, a novel large-animal model of HT1, devel

5 iously proposed based on recently determined FAH crystal structures.

6 deficiency of fumarylacetoacetate hydrolase (FAH) and develop progressive hepatocellular dysfunction

7 deficiency of fumarylacetoacetate hydrolase (FAH) and homogentisic acid dioxygenase (HGD), respective

8 Fumarylacetoacetate hydrolase (FAH) catalyzes the hydrolytic cleavage of a carbon-carbo

9 for MAAI and fumarylacetoacetate hydrolase (FAH) died rapidly on a normal diet, indicating that MAA

10 Fumarylacetoacetate hydrolase (FAH) domain-containing proteins occur in both prokaryote

11 ansferred the fumarylacetoacetate hydrolase (FAH) gene by LV vectors into FAH((-/-)) mice (n = 97) an

12 in the human fumarylacetoacetate hydrolase (FAH) gene that disrupt tyrosine catabolism.

13 member of the fumarylacetoacetate hydrolase (FAH) superfamily and implicated Glu-109 and Glu-111 as p

14 deficiency of fumarylacetoacetate hydrolase (FAH), to determine whether in vivo selection of correcte

15 in the enzyme fumarylacetoacetate hydrolase (FAH).

16 the pathway, fumarylacetoacetate hydrolase (FAH).

17 elective repopulation of the liver occurs in FAH-deficient mice.

18 tate hydrolase (FAH) gene by LV vectors into FAH((-/-)) mice (n = 97) and performed serial hepatocyte

19 Under conditions of low-dose NTBC, FAH(-/-) pigs developed liver fibrosis and portal hypert

20 The analysis of FAH structures corresponding to different catalytic stat

21 ight into the structure-based development of FAH inhibitors.

22 We expect that the subsequent generation of FAH-null homozygote pigs will serve as a significant adv

23 n of the K10C2.4, which encodes a homolog of FAH.

24 ntial human metabolic function, with loss of FAH activity causing the fatal metabolic disease heredit

25 The crystal structure of FAH complexed with HMPOBA refined at 1.3-A resolution re

26 Because HGD is upstream of FAH in the tyrosine pathway, mice doubly mutant in both

27 o structural differences in their respective FAH domains; however, the precise relationship between s

28 In conclusion, the FAH(-/-) pig is a large-animal model of HT1 with clinica

29 oxy transition state intermediate during the FAH catalyzed reaction, and reveals a Mg(2+) bound in th

30 injection of adult bone marrow cells in the FAH(-/-) mouse, an animal model of tyrosinemia type I, r

31 recise relationship between structure of the FAH domain and the associated enzyme function remains el

32 in vivo from a luciferase gene linked to the FAH gene.

33 In mammals, three FAH domain-containing proteins, FAHD1, FAHD2A, and FAHD2

34 er where they differentiated into areas with FAH and Albumin positive hepatocytes.

35 Conclusion: Coexpression with FAH is an effective technique for lifelong expression of

36 odules and total liver from the patient with FAH deficiency were compared with control donor liver.

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