ArticleJournal of inherited metabolic disease2018
Correlation between the molecular effects of mutations at the dimer interface of alanine-glyoxylate aminotransferase leading to primary hyperoxaluria type I and the cellular response to vitamin B
Article in Journal of inherited metabolic disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 30 citations in OpenAlex.
- Lumasiran at birth changes the trajectory of primary hyperoxaluria type 1: same disease, different outcomes in two affected siblings.Journal of nephrology · 2025Article
- Real-Life Data of 2-Year Lumasiran Use in the DAILY-LUMA Cohort.Kidney international reports · 2025Article
- Oxalate homeostasis.Nature reviews. Nephrology · 2023Review
- The effect of lumasiran therapy for primary hyperoxaluria type 1 in small infants.Pediatric nephrology (Berlin, Germany) · 2022Article
- Perspectives in primary hyperoxaluria - historical, current and future clinical interventions.Nature reviews. Urology · 2022Review
- Primary hyperoxaluria diagnosed after kidney transplantation: a case report and literature review.BMC nephrology · 2021Review
- Small Molecule-Based Enzyme Inhibitors in the Treatment of Primary Hyperoxalurias.Journal of personalized medicine · 2021Review
- Novel mutations in response to vitamin B6 in primary hyperoxaluria type 1 after only kidney transplantation: a case report.Translational andrology and urology · 2020Article
- Modulation of Guanylate Cyclase Activating Protein 1 (GCAP1) Dimeric Assembly by CaBiomolecules · 2020Article
- Molecular basis of primary hyperoxaluria: clues to innovative treatments.Urolithiasis · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Primary hyperoxaluria type I (PH1) is a rare disease caused by the deficit of liver alanine-glyoxylate aminotransferase (AGT). AGT prevents oxalate formation by converting peroxisomal glyoxylate to glycine. When the enzyme is deficient, progressive calcium oxalate stones deposit first in the urinary tract and then at the systemic level. Pyridoxal 5'-phosphate (PLP), the AGT coenzyme, exerts a chaperone role by promoting dimerization, as demonstrated by studies at protein and cellular level. Thus, variants showing a destabilized dimeric structure should, in principle, be responsive to vitamin B
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.