ArticleBiochemistry2022
ALAD Inhibition by Porphobilinogen Rationalizes the Accumulation of δ-Aminolevulinate in Acute Porphyrias.
Article in Biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Updates to gene-disease classifications and inheritance patterns for porphyrias.Molecular genetics and metabolism · 2026Article
- Aminolevulinate inhibition of human coproporphyrinogen oxidase clarifies coproporphyrin III accumulation in porphyrias.Bioscience reports · 2026Article
- Liver Transplantation and Other Hepatically Directed Therapies Do Not Change the Biochemical Phenotype nor Halt Progression of Leukodystrophy due to BiallelicJIMD reports · 2026Article
- Clinical Features and Outcomes of Acute Intermittent Porphyria Presenting With Acute Quadriparesis: A Case Series and Follow-Up Study.European journal of neurology · 2025Article
- Systematically testing human HMBS missense variants to reveal mechanism and pathogenic variation.American journal of human genetics · 2023Article
- Systematically testing human HMBS missense variants to reveal mechanism and pathogenic variation.bioRxiv : the preprint server for biology · 2023Article
- Protoporphyrin IX Binds to Iron(II)-Loaded and to Zinc-Loaded Human Frataxin.Life (Basel, Switzerland) · 2023Article
- 5-aminolevulinate and CHIL3/CHI3L1 treatment amid ischemia aids liver metabolism and reduces ischemia-reperfusion injury.Theranostics · 2023Article
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Authors and funding
10 authors at 4 institutions in 1 country.
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Abstract
Patients with major forms of acute hepatic porphyria present acute neurological attacks with overproduction of porphobilinogen (PBG) and δ-aminolevulinic acid (ALA). Even if ALA is considered the most likely agent inducing the acute symptoms, the mechanism of its accumulation has not been experimentally demonstrated. In the most frequent form, acute intermittent porphyria (AIP), inherited gene mutations induce a deficiency in PBG deaminase; thus, accumulation of the substrate PBG is biochemically obligated but not that of ALA. A similar scenario is observed in other forms of acute hepatic porphyria (i.e., porphyria variegate, VP) in which PBG deaminase is inhibited by metabolic intermediates. Here, we have investigated the molecular basis of δ-aminolevulinate accumulation using
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