ReviewDrug metabolism reviews2008
Structure-function analyses of single nucleotide polymorphisms in human N-acetyltransferase 1.
Review in Drug metabolism reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
13 citing papers in PubMed, 49 citations in OpenAlex.
- Human disposition, metabolism and excretion of etamicastat, a reversible, peripherally selective dopamine β-hydroxylase inhibitor.British journal of clinical pharmacology · 2014Trial
- Safety, tolerability, and pharmacokinetics of etamicastat, a novel dopamine-β-hydroxylase inhibitor, in a rising multiple-dose study in young healthy subjects.Drugs in R&D · 2010Trial
- Mesalazine pharmacokinetics and NAT2 phenotype.European journal of clinical pharmacology · 2009Trial
- Associations of Cruciferous Vegetable Intake with Breast Cancer Survival in a Diverse Population in the Pathways Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025Article
- Bioactivation, Mutagenicity, DNA Damage, and Oxidative Stress Induced by 3,4-Dimethylaniline.Biomolecules · 2024Article
- Identification and characterization of potent, selective, and efficacious inhibitors of human arylamine N-acetyltransferase 1.Archives of toxicology · 2022Article
- Acetyl coenzyme A kinetic studies onFrontiers in pharmacology · 2022Article
- Arylamine N-acetyltransferases: from drug metabolism and pharmacogenetics to drug discovery.British journal of pharmacology · 2014Review
- Arylamine N-acetyltransferases: a structural perspective.British journal of pharmacology · 2013Review
- Phenotype of the most common "slow acetylator" arylamine N-acetyltransferase 1 genetic variant (NAT1*14B) is substrate-dependent.Drug metabolism and disposition: the biological fate of chemicals · 2012Article
- Functional effects of genetic polymorphisms in the N-acetyltransferase 1 coding and 3' untranslated regions.Birth defects research. Part A, Clinical and molecular teratology · 2011Article
- N-acetyltransferase SNPs: emerging concepts serve as a paradigm for understanding complexities of personalized medicine.Expert opinion on drug metabolism & toxicology · 2009Review
- FAF-Drugs2: free ADME/tox filtering tool to assist drug discovery and chemical biology projects.BMC bioinformatics · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human N-acetyltransferase 1 (NAT1) alleles are characterized by one or more single nucleotide polymorphisms (SNPs) associated with rapid and slow acetylation phenotypes. NAT1 both activates and deactivates arylamine drugs and carcinogens, and NAT1 polymorphisms are associated with increased frequencies of many cancers and birth defects. The recently resolved human NAT1 crystal structure was used to evaluate SNPs resulting in the protein substitutions R64W, V149I, R187Q, M205V, S214A, D251V, E261K, and I263V. The analysis enhances knowledge of NAT1 structure-function relationships, important for understanding associations of NAT1 SNPs with genetic predisposition to cancer, birth defects, and other diseases.
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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.