ORIGINAL ARTICLESDebrisoquine hydroxylase gene polymorphism and susceptibility to Parkinson's disease
References (35)
- et al.
Multiple mutations of the human cytochrome P450IID6 gene (CYP2D6) in poor metabolizers of debrisoquine
J Biol Chem
(1990) - et al.
Ecogenetics of Parkinson's disease: 4-hydroxylation of debrisoquine
Lancet
(1985) - et al.
Debrisoquine metabolism in Parkinsonian patients treated with antihistamine drugs
Lancet
(1987) - et al.
Genetic analysis of cytochrome P450 gene loci
Methods Enzymol
(1991) - et al.
Detection of debrisoquine hydroxylation phenotypes
Lancet
(1990) - et al.
Etiology of Parkinson's disease
Lancet
(1983) - et al.
Inhibition of NADH-linked oxidation in brain mitochondria by MPP+, a metabolite of the neurotoxin MPTP
Life Sci
(1985) - et al.
4'-alkylated analogs of MPP + are potent inhibitors of mitochondrial respiration
Biochem Biophys Res Commun
(1990) - et al.
MPTP the neurotoxin inducing Parkinson's disease, is a potent inhibitor of human and rat P450 enzymes (P450bufl, P450db1) catalyzing debrisoquine 4-hydroxylation
Biochem Biophys Res Commun
(1987) - et al.
The genetic polymorphism of debrisoquine/ sparteine metabolism—clinical aspects
Pharmacol Ther
(1990)
Metabolic factors in cancer susceptibility
Cancer Surv
The genetics of Parkinson's disease
Neurology
Genetic susceptibility to Parkinson's disease
Neurology
A family and population study of the genetic polymorphism of debrisoquine oxidation in a white British population
J Med Genet
Identification of the primary gene defect at the cytochrome P450 CYP2D6 locus
Nature
The human CYP2D6 locus associated with a common genetic defect in drug oxidation: a G1943 to A base change in intron 3 of a mutant CYP2D6 allele results in an aberrrant 3' splice recognition site.
Am J Hum Genet
Deletion of the entire CYP2D6 gene as a cause of impaired drug metabolism in poor metabolizers of the debrisoquine/sparteine polymorphism
Am J Hum Genet
Cited by (440)
Association of cytochrome P2D6 gene polymorphism with the susceptibility of Egyptian patients to systemic sclerosis disease
2021, Meta GeneCitation Excerpt :Patients full medical histories were taken and the physical examinations were carried out, including: general, cutaneous, vascular, musculoskeletal, pulmonary, cardiac, gastrointestinal, and neurological examinations.Tests were conducted, including renal, liver function tests, antinuclear antibody (ANA) titer and pattern, anti scleroderma 70, high-resolution computer tomography (HRCT), pulmonary function tests (PFT), and cardiac echocardiography. CYP2D6 gene alleles (CYP2D6 *1, CYP2D6 *3, and CYP2D6 *4) were determined according to the technique described by Smith et al. (Smith et al., 1992), using the PCR-RFLP (polymerasechain reaction-restriction fragment length polymorphism) method. Genomic DNAwas isolated from the peripheral blood leukocytes using the mini kit purchased from INTRONBIO (ANALSIS) Catalog No: 17045.
Significance of the genetic polymorphism of CYP2D6 and NAT2 in patients with inflammatory bowel diseases
2014, Pharmacological ReportsThe relationship between plasma concentration of metoprolol and CYP2D6 genotype in patients with ischemic heart disease
2014, Pharmacological ReportsCitation Excerpt :Each subject agreed to sign a written informed consent. The blood samples were analyzed for two major defective alleles for the CYP2D6 gene – CYP2D6*4 and CYP2D6*3 – by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method according to the procedure proposed by Smith et al. [8]. DNA was arranged from leukocytes extracted from peripheral blood.
CYP2D6 phenotypes and Parkinson's disease risk: A meta-analysis
2014, Journal of the Neurological SciencesCitation Excerpt :Meta-regression analysis showed that the source of the controls was the major factor contributing to heterogeneity (regression coefficient = − 0.263; 95%CI: − 472–0.053; P = 0.015). When the sensitivity analysis was conducted, our results indicated that the study by Smith [7] apparently influenced the overall results. After excluding that study from the analysis, the pooled ORs (95%CI) of the remaining studies were still insignificant (OR: 1.03, 95%CI: 0.95–1.12; P = 0.515), and there was still significant heterogeneity (I2 = 32.0%, P = 0.002).