ArticleThe Journal of biological chemistry2017
Fumarylacetoacetate Hydrolase Knock-out Rabbit Model for Hereditary Tyrosinemia Type 1.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Overexpression of alcohol dehydrogenase 1 A inhibits the progress of triple negative breast cancer via Wnt/β-catenin signaling.Scientific reports · 2025Article
- Evaluation of guide-free Cas9-induced genomic damage and transcriptome changes in pig embryos.Molecular therapy. Nucleic acids · 2023Article
- Toxic Metabolites and Inborn Errors of Amino Acid Metabolism: What One Informs about the Other.Metabolites · 2022Review
- Decreased SLC27A5 Suppresses Lipid Synthesis and Tyrosine Metabolism to Activate the Cell Cycle in Hepatocellular Carcinoma.Biomedicines · 2022Article
- Subproteomic profiling from renal cortices in OLETF rats reveals mutations of multiple novel genes in diabetic nephropathy.Genes & genomics · 2022Article
- Borrelia burgdorferi infection modifies protein content in saliva of Ixodes scapularis nymphs.BMC genomics · 2021Article
- CRISPR/Cas9-Mediated Gene Correction in Newborn Rabbits with Hereditary Tyrosinemia Type I.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Genetically Modified Rabbits for Cardiovascular Research.Frontiers in genetics · 2021Review
- Review
- Genome engineering technologies in rabbits.Journal of biomedical research · 2020Article
- Principles and Applications of Rabbit Models for Atherosclerosis Research.Journal of atherosclerosis and thrombosis · 2018Review
Corrections and comments
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Authors and funding
24 authors at 10 institutions in 4 countries.
Funding
Abstract
Hereditary tyrosinemia type 1 (HT1) is a severe human autosomal recessive disorder caused by the deficiency of fumarylacetoacetate hydroxylase (FAH), an enzyme catalyzing the last step in the tyrosine degradation pathway. Lack of FAH causes accumulation of toxic metabolites (fumarylacetoacetate and succinylacetone) in blood and tissues, ultimately resulting in severe liver and kidney damage with onset that ranges from infancy to adolescence. This tissue damage is lethal but can be controlled by administration of 2-(2-nitro-4-trifluoromethylbenzoyl)-1,3-cyclohexanedione (NTBC), which inhibits tyrosine catabolism upstream of the generation of fumarylacetoacetate and succinylacetone. Notably, in animals lacking FAH, transient withdrawal of NTBC can be used to induce liver damage and a concomitant regenerative response that stimulates the growth of healthy hepatocytes. Among other things, this model has raised tremendous interest for the
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Registered trials
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