Catechol O-Methyltransferase
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Subject Areas on Research
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(3H)norepinephrine binding: unrelated to catechol-O-methyl transferase.
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A replicated molecular genetic basis for subtyping antisocial behavior in children with attention-deficit/hyperactivity disorder.
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Age-Dependent Effects of Catechol-O-Methyltransferase (COMT) Gene Val158Met Polymorphism on Language Function in Developing Children.
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Assessing potential functionality of catechol-O-methyltransferase (COMT) polymorphisms associated with pain sensitivity and temporomandibular joint disorders.
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Association analysis of the COMT/MTHFR genes and geriatric depression: an MRI study of the putamen.
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Associations Between Catecholaminergic and Serotonergic Genes and Persistent Arm Pain Severity Following Breast Cancer Surgery.
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Biopsychosocial Influences on Shoulder Pain: Analyzing the Temporal Ordering of Postoperative Recovery.
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Biopsychosocial influence on exercise-induced delayed onset muscle soreness at the shoulder: pain catastrophizing and catechol-o-methyltransferase (COMT) diplotype predict pain ratings.
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Biopsychosocial influence on exercise-induced injury: genetic and psychological combinations are predictive of shoulder pain phenotypes.
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Biopsychosocial influence on shoulder pain: Rationale and protocol for a pre-clinical trial.
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COMT Diplotype Amplifies Effect of Stress on Risk of Temporomandibular Pain.
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COMT Val(158) Met genotype is associated with reward learning: a replication study and meta-analysis.
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COMT Val158Met Polymorphism, Cardiometabolic Risk, and Nadir CD4 Synergistically Increase Risk of Neurocognitive Impairment in Men Living With HIV.
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COMT and anxiety and cognition in children with chromosome 22q11.2 deletion syndrome.
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COMT gene locus: new functional variants.
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COMT val108/158 met genotype affects neural but not cognitive processing in healthy individuals.
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COMT158 polymorphism and hostility.
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Catechol O-methyltransferase haplotype predicts immediate musculoskeletal neck pain and psychological symptoms after motor vehicle collision.
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Catechol O-methyltransferase in red blood cells of schizophrenic, depressed, and normal human subjects.
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Catechol O-methyltransferase val158-met genotype and individual variation in the brain response to amphetamine.
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Catechol O-methyltransferase val158met genotype and neural mechanisms related to affective arousal and regulation.
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Catechol-O-methyltransferase activity and classification of depression.
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Catechol-O-methyltransferase and breast cancer risk.
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Catechol-O-methyltransferase gene polymorphisms are associated with multiple pain-evoking stimuli.
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Catechol-O-methyltransferase genotype predicts pain severity in hospitalized burn patients.
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Catechol-O-methyltransferase inhibition alters pain and anxiety-related volitional behaviors through activation of β-adrenergic receptors in the rat.
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Characterization of NF-kB-mediated inhibition of catechol-O-methyltransferase.
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Clinical Pharmacogenetics Implementation Consortium Guideline for CYP2D6, OPRM1, and COMT Genotypes and Select Opioid Therapy.
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Cognitive correlates of a functional COMT polymorphism in children with 22q11.2 deletion syndrome.
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Complex multilocus effects of catechol-O-methyltransferase haplotypes predict pain and pain interference 6 weeks after motor vehicle collision.
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Comt1 genotype and expression predicts anxiety and nociceptive sensitivity in inbred strains of mice.
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Disruptive mRNA folding increases translational efficiency of catechol-O-methyltransferase variant.
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Divergence of an association between depressive symptoms and a dopamine polygenic score in Caucasians and Asians.
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Effect of catechol-O-methyltransferase polymorphism on response to propranolol therapy in chronic musculoskeletal pain: a randomized, double-blind, placebo-controlled, crossover pilot study.
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Epistasis between polymorphisms in COMT, ESR1, and GCH1 influences COMT enzyme activity and pain.
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Estrogen metabolism within the lung and its modulation by tobacco smoke.
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Evidence for a biopsychosocial influence on shoulder pain: pain catastrophizing and catechol-O-methyltransferase (COMT) diplotype predict clinical pain ratings.
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Evidence for monozygotic twin (MZ) discordance in methylation level at two CpG sites in the promoter region of the catechol-O-methyltransferase (COMT) gene.
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Genetic basis for individual variations in pain perception and the development of a chronic pain condition.
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Genetic variants in 5-HTTLPR, BDNF, HTR1A, COMT, and FKBP5 and risk for treated depression after cancer diagnosis.
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Genetic variation in components of dopamine neurotransmission impacts ventral striatal reactivity associated with impulsivity.
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Genetic vulnerability to affective psychopathology in childhood: a combined voxel-based morphometry and functional magnetic resonance imaging study.
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Haplotype associations with quantitative traits in the presence of complex multilocus and heterogeneous effects.
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Human Genetic Variability Contributes to Postoperative Morphine Consumption.
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Human catechol-O-methyltransferase haplotypes modulate protein expression by altering mRNA secondary structure.
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Identification of neurogenetic pathways of risk for psychopathology.
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Imaging genomics.
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Increased corpus callosum volume in children with chromosome 22q11.2 deletion syndrome is associated with neurocognitive deficits and genetic polymorphisms.
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Influence of psychological factors on risk of temporomandibular disorders.
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Janus molecule I: dichotomous effects of COMT in neuropathic vs nociceptive pain modalities.
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Low catechol-O-methyltransferase and stress potentiate functional pain and depressive behavior, especially in female mice.
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Low enzymatic activity haplotypes of the human catechol-O-methyltransferase gene: enrichment for marker SNPs.
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Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene X environment interaction.
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Modification of COMT-dependent pain sensitivity by psychological stress and sex.
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Modification of depression by COMT val158met polymorphism in children exposed to early severe psychosocial deprivation.
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Molecular genetic mechanisms of allelic specific regulation of murine Comt expression.
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Monoamine oxidase and catechol-O-methyltransferase activity in hamster and rat insulinomas.
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Neurocognitive correlates of the COMT Val(158)Met polymorphism in chronic schizophrenia.
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Neurocognitive effects of transcranial direct current stimulation (tDCS) in unipolar and bipolar depression: Findings from an international randomized controlled trial.
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Nuclear factor-kappa B regulates pain and COMT expression in a rodent model of inflammation.
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Pain modality- and sex-specific effects of COMT genetic functional variants.
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Persistent Catechol-O-methyltransferase-dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors.
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Prefrontal-hippocampal coupling during memory processing is modulated by COMT val158met genotype.
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Red blood cell catechol O-methyl transferase and response to imipramine in unipolar depressive women.
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Results of a pilot multicenter genotype-based randomized placebo-controlled trial of propranolol to reduce pain after major thermal burn injury.
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Serotonin-induced hypersensitivity via inhibition of catechol O-methyltransferase activity.
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Stress, COMT Polymorphisms, and Depressive Symptoms in Older Australian Women: An Exploratory Study.
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Stressful life events, perceived stress, and 12-month course of geriatric depression: direct effects and moderation by the 5-HTTLPR and COMT Val158Met polymorphisms.
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Structural mechanism of S-adenosyl methionine binding to catechol O-methyltransferase.
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Sustained stimulation of β2- and β3-adrenergic receptors leads to persistent functional pain and neuroinflammation.
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The COMT Val158Met polymorphism and cognition in depressed and nondepressed older adults.
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The COMT Val158Met polymorphism and temporal lobe morphometry in healthy adults.
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The what, where, and when of catechol-O-methyltransferase.
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Uncovering precision phenotype-biomarker associations in traumatic brain injury using topological data analysis.
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Vitamin D inhibits proliferation of human uterine leiomyoma cells via catechol-O-methyltransferase.
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β2- and β3-adrenergic receptors drive COMT-dependent pain by increasing production of nitric oxide and cytokines.