ArticleJIMD reports2021
Expression of tyrosine pathway enzymes in mice demonstrates that homogentisate 1,2-dioxygenase deficiency in the liver is responsible for homogentisic acid-derived ochronotic pigmentation.
Article in JIMD reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- iTRAQ- and MRM-Based Proteomics Identify Early Injury Biomarkers for Primary Dysfunction After Liver Transplantation.Annals of transplantation · 2026Article
- Specific knockout of kidney homogentisate 1,2-dioxygenase reveals that local metabolism of tyrosine and homogentisic acid is negligible in alkaptonuria.Human molecular genetics · 2026Article
- A Comprehensive In Vitro and In Silico Approach for Targeting 4-Hydroxyphenyl Pyruvate Dioxygenase: Towards New Therapeutics for Alkaptonuria.International journal of molecular sciences · 2025Article
- A temporal single cell transcriptome atlas of zebrafish anterior segment development.Scientific reports · 2023Article
- Determinants of tyrosinaemia during nitisinone therapy in alkaptonuria.Scientific reports · 2022Article
- Impact of Nitisinone on the Cerebrospinal Fluid Metabolome of a Murine Model of Alkaptonuria.Metabolites · 2022Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alkaptonuria (AKU) is caused by homogentisate 1,2-dioxygenase (HGD) deficiency. This study aimed to determine if HGD and other enzymes related to tyrosine metabolism are associated with the location of ochronotic pigment. Liver, kidney, skin, bone, brain, eyes, spleen, intestine, lung, heart, cartilage, and muscle were harvested from 6 AKU BALB/c
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Registered trials
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