Kidneys of Mice With Hereditary Tyrosinemia Type I Are Extremely Sensitive to Cytotoxicity

No abstract is available for this paper.

• Publication year

  2006

• Venue

  Pediatric Research

• Publication date

  2006-03-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1203/01.pdr.0000198810.57642.b4PMID 16492973
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Tyrosinemia

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• Protective effects of long term dietary restriction on swimming exercise‐induced oxidative stress in the liver, heart and kidney of rat

  2007cited by this paper
• Hepatocellular carcinoma in hereditary tyrosinemia type I despite 2-(2 nitro-4-3 trifluoro- methylbenzoyl)-1, 3-cyclohexanedione treatment.

  2005influential reference
• Renal proximal tubular cells acquire resistance to cell death stimuli in mice with hereditary tyrosinemia type 1.

  2004cited by this paper
• Chronic liver disease in murine hereditary tyrosinemia type 1 induces resistance to cell death

  2004cited by this paper
• Extensive changes in liver gene expression induced by hereditary tyrosinemia type I are not normalized by treatment with 2-(2-nitro-4-trifluoromethylbenzoyl)-1,3-cyclohexanedione (NTBC).

  2003cited by this paper
• Fumarylacetoacetate, the metabolite accumulating in hereditary tyrosinemia, activates the ERK pathway and induces mitotic abnormalities and genomic instability.

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• The Pathophysiology and Treatment of Hereditary Tyrosinemia Type 1

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• Tyrosinemia: A Review

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• The Nephropathy of Type I Tyrosinemia after Liver Transplantation

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• SIADH as an Underrecognized Manifestation of Porphyria-like Crises in Hereditary Tyrosinemia Type 1: Clinical and Pathophysiological Insights

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