Alanine-glyoxylate aminotransferase-deficient mice, a model for primary hyperoxaluria that responds to adenoviral gene transfer
Author:
Publisher
Proceedings of the National Academy of Sciences
Subject
Multidisciplinary
Reference26 articles.
1. Oxalate nephropathy in a Tibetan Spaniel litter. A probable case of primary hyperoxaluria
2. Animal models of kidney stone formation: an analysis
3. The Mouse Alanine:Glyoxylate Aminotransferase Gene (Agxt1): Cloning, Expression, and Mapping to Chromosome 1
4. Characteristics of hepatic alanine-glyoxylate aminotransferase in different mammalian species
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1. Restored glyoxylate metabolism after AGXT gene correction and direct reprogramming of primary hyperoxaluria type 1 fibroblasts;iScience;2024-04
2. Efficient and safe therapeutic use of paired Cas9-nickases for primary hyperoxaluria type 1;EMBO Molecular Medicine;2024-01-05
3. Therapeutic targeting of HYPDH/PRODH2 with N-propargylglycine offers a Hyperoxaluria treatment opportunity;Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease;2024-01
4. Ovarian cancer G protein-coupled receptor 1 deficiency exacerbates crystal deposition and kidney injury in oxalate nephropathy in female mice;Clinical Science;2023-07
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