ArticleProceedings of the National Academy of Sciences of the United States of America2006
Alanine-glyoxylate aminotransferase-deficient mice, a model for primary hyperoxaluria that responds to adenoviral gene transfer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
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Who cites it
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.
- Loss of alanine-glyoxylate and serine-pyruvate aminotransferase expression accelerated the progression of hepatocellular carcinoma and predicted poor prognosis.Journal of translational medicine · 2019Pooled it
- Animal Models of Hyperoxaluria and Their Relevance for Fundamental Research and Clinical Practice.International journal of molecular sciences · 2026Review
- Rapid multiplex liver gene-editing in mice using adeno-associated virus 8 or lipid nanoparticles.Molecular therapy. Advances · 2026Article
- Animal models for calcium oxalate kidney stone research.Zoological research · 2026Review
- Novel AAV843 Vector-Mediated Gene Replacement Therapy Rescues Primary Hyperoxaluria Type I in Mice.Cells · 2026Article
- LNP-mediated in vivo base editing corrects Agxt to cure primary hyperoxaluria type 1.Clinical and translational medicine · 2025Article
- Normal urinary oxalate excretion in 4-hydroxy-2-oxo-glutarate aldolase 1 (HOGA1) deficient mice with AGT expression in peroxisomes and not in mitochondria.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Characterization of CHK-336, A First-in-Class, Liver-Targeted, Small-Molecule Lactate Dehydrogenase Inhibitor for Hyperoxaluria Treatment.Journal of the American Society of Nephrology : JASN · 2025Article
- Efficient and safe in vivo treatment of primary hyperoxaluria type 1 via LNP-CRISPR-Cas9-mediated glycolate oxidase disruption.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- A mouse model for the study of diet-induced changes in intestinal microbiome composition on renal calcium oxalate crystal formation.Urolithiasis · 2024Article
- Lipid nanoparticle-mediated base-editing of the Hao1 gene achieves sustainable primary hyperoxaluria type 1 therapy in rats.Science China. Life sciences · 2024Article
- Discovery of l-Lysine Dioxalate (LH1513) as a Novel Inhibitor of Calcium Oxalate Crystallization for Hyperoxaluria.ACS medicinal chemistry letters · 2024Article
- Inhibition of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis.Nature metabolism · 2024Article
- Restored glyoxylate metabolism after AGXT gene correction and direct reprogramming of primary hyperoxaluria type 1 fibroblasts.iScience · 2024Article
- Therapeutic targeting of HYPDH/PRODH2 with N-propargylglycine offers a Hyperoxaluria treatment opportunity.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Efficient and safe therapeutic use of paired Cas9-nickases for primary hyperoxaluria type 1.EMBO molecular medicine · 2024Article
- Multiplex gene editing reduces oxalate production in primary hyperoxaluria type 1.Zoological research · 2023Article
- Mouse Models to Study Peroxisomal Functions and Disorders: Overview, Caveats, and Recommendations.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Article
- Two independent modes of kidney stone suppression achieved by AIM/CD5L and KIM-1.Communications biology · 2022Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Mutations in the alanine-glyoxylate amino transferase gene (AGXT) are responsible for primary hyperoxaluria type I, a rare disease characterized by excessive hepatic oxalate production that leads to renal failure. We generated a null mutant mouse by targeted mutagenesis of the homologous gene, Agxt, in embryonic stem cells. Mutant mice developed normally, and they exhibited hyperoxaluria and crystalluria. Approximately half of the male mice in mixed genetic background developed calcium oxalate urinary stones. Severe nephrocalcinosis and renal failure developed after enhancement of oxalate production by ethylene glycol administration. Hepatic expression of human AGT1, the protein encoded by AGXT, by adenoviral vector-mediated gene transfer in Agxt(-/-) mice normalized urinary oxalate excretion and prevented oxalate crystalluria. Subcellular fractionation and immunofluorescence studies revealed that, as in the human liver, the expressed wild-type human AGT1 was predominantly localized in mouse hepatocellular peroxisomes, whereas the most common mutant form of AGT1 (G170R) was localized predominantly in the mitochondria.
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