Biochemical and Biophysical Research Communications
Regular ArticleCatecholestrogen Sulfation: Possible Role in Carcinogenesis☆
References (52)
- et al.
Variations in catechol O-methyltransferase activity in inbred strains of rats
Neuropharmacology
(1977) - et al.
Phenol sulfotransferase pharmacogenetics in humans: Association of common SULT1A1 alleles with TS PST phenotype
Biochem. Biophys. Res. Commun.
(1997) - et al.
Human cytosolic sulphotransferases: Genetics, characteristics, toxicological aspects
Mutat. Res.
(2001) - et al.
Human liver estrogen sulfotransferase: cDNA cloning, expression and biochemical characterization
Biochem. Biophys. Res. Commun.
(1994) - et al.
Human hydroxysteroid sulfotransferase SULT2B1: Two enzymes encoded by a single chromosome 19 gene
Genomics
(1998) - et al.
Human liver phenol sulfotransferase: Assay conditions, biochemical properties and partial purification of isozymes of the thermostable form
Biochem. Pharmacol.
(1987) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein–dye binding
Anal. Biochem.
(1976)- et al.
Molecular cloning, expression, and characterization of novel human SULT1C sulfotransferases that catalyze the sulfonation of N-hydroxy-2-acetylaminofluorene
J. Biol. Chem.
(1998) - et al.
Gas chromatography/mass spectrometry of catechol estrogens
Steroids
(1992) - et al.
High metabolization of catecholestrogens by type 1 estrogen sulfotransferase (hEST1)
J. Steroid Biochem. Mol. Biol.
(2001)
A biomathematical model of breast cancer incidence: The contribution of reproductive factors to variation in breast cancer incidence
Hormones and mammary carcinogenesis in mice, rats and humans: A unifying hypothesis
Proc. Natl. Acad. Sci. USA
Alterations within the estrogen receptor in breast cancer
Mechanism of metabolic activation and inactivation of catecholestrogens: A basis of genotoxicity
Polycyclic Aromatic Compounds
Molecular mechanisms of estrogen carcinogenesis
Annu. Rev. Pharmacol. Toxicol.
Molecular origin of cancer: Catechol estrogen-3,4-quinones as endogenous tumor initiators
Proc. Natl. Acad. Sci. USA
p-Quinone methides are the major decomposition products of catecholestrogen O-quinones
Carcinogenesis
Conversion of estrone to 2- and 4-hydroxyestrone by hamster kidney and liver microsomes: Implications for the mechanism of estrogen-induced carcinogenesis
Endocrinology
Linkage relationships between a major gene for catechol-O-methyltransferase activity and 25 polymorphic marker systems
Am. J. Med. Genet.
Human liver catechol O-methyltransferase pharmacogenetics
Clin. Pharmacol. Ther.
Methylation pharmacogenetics: Catechol O-methyltransferase, thiopurine methyltransferase, and histamine N-methyltransferase
Annu. Rev. Pharmacol. Toxicol.
An association between the allele coding for a low activity variant of catechol O-methyltransferase and the risk for breast cancer
Cancer Res.
Genetic polymorphisms in catechol O-methyltransferase, menopausal status, and breast cancer risk
Cancer Res.
Polymorphic catechol-O-methyltransferase gene and breast cancer risk
Cancer Epidemiol. Biomarkers Prev.
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2022, Drug Discovery TodayCitation Excerpt :It was previously suggested that a large dynamic shift of L3 occurs upon PAPS binding to allow large ligands to enter into the active site, whereas this is not necessarily required for small compounds to dock.108 Remarkably, decreased sulfation has been reported for several large ligands (epicatechin, chrysin, resveratrol, quercetin, 2OHE2, and E2) for SULT1A1*3 compared with WT according to the Vmax values, whereas increased affinities can be expected according to the observed Vmax/Km values (Table 2).82 The slightly increased flexibility of the L3 region in the case of SULT1A1*3 detected by our simulations (Fig. 2b) likely facilitates the entering of large ligands, accounting for their higher affinity, whereas it destabilizes PAPS binding, explaining the slightly decreased sulfation activity observed.
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Supported in part by NIH Grants RO1 GM28157 (R.M.W.), RO1 GM35720 (R.M.W.), UO1 GM61388 (R.M.W.), and DAMD 17-99-1-9281 (A.A.A.).
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