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anti-Human COMT Antibodies:
anti-Mouse (Murine) COMT Antibodies:
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Human Monoclonal COMT Primary Antibody for WB - ABIN1882224
Zeng, Ye, Lu, Chua, Tan, Zhong: Chiral Brønsted acid catalyzed enantioselective addition of alpha-isocyanoacetamides to aldehydes. in Organic letters 2010
Show all 5 Pubmed References
Mouse (Murine) Monoclonal COMT Primary Antibody for BI, IF - ABIN968704
Gogos, Morgan, Luine, Santha, Ogawa, Pfaff, Karayiorgou: Catechol-O-methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior. in Proceedings of the National Academy of Sciences of the United States of America 1998
Show all 3 Pubmed References
Human Polyclonal COMT Primary Antibody for ELISA, WB - ABIN250484
Yao, Harris, Zhang: Intrarenal dopamine attenuates deoxycorticosterone acetate/high salt-induced blood pressure elevation in part through activation of a medullary cyclooxygenase 2 pathway. in Hypertension (Dallas, Tex. : 1979) 2009
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Human Polyclonal COMT Primary Antibody for EIA, ELISA - ABIN188559
Tunbridge, Harrison, Weinberger: Catechol-o-methyltransferase, cognition, and psychosis: Val158Met and beyond. in Biological psychiatry 2006
Human Polyclonal COMT Primary Antibody for WB - ABIN514522
Hevir, Sinkovec, Rižner: Disturbed expression of phase I and phase II estrogen-metabolizing enzymes in endometrial cancer: lower levels of CYP1B1 and increased expression of S-COMT. in Molecular and cellular endocrinology 2010
Human Polyclonal COMT Primary Antibody for IHC, IHC (p) - ABIN4299996
Hirata, Hinoda, Okayama, Suehiro, Kawamoto, Kikuno, Rabban, Chen, Dahiya: COMT polymorphisms affecting protein expression are risk factors for endometrial cancer. in Molecular carcinogenesis 2008
there is a relationship between Val158Met COMT and certain social cognitive deficits in patients with schizophrenia
meta-analysis suggested that the COMT Val158Met polymorphism was not associated with migraine risk (Meta-Analysis)
These findings support the hypothesis of a broad effect of the Val158Met polymorphism in the COMT gene on several dimensions of behavior and neuropsychiatric symptoms.
In our study, statistical analysis has showed that in control group Val/Met COMT genotype was significantly higher compared with the obesity group
COMT 158G/A (COMT Val158Met) polymorphism was associated with suicide susceptibility only in females.
Early life adversity and COMT polymorphism gene by environment (G x E) interaction on stress reactivity in adulthood.
The COMT rs4680 Met allele carriers (Met/Met and Met/Val genotypes) is twice as likely to have a history of concussion compared to other genotypes.
3-way interaction of MTHFR (show MTHFR Antibodies) C677T, COMT Val158Met and childhood adversity increases risk of schizophrenia.
Receiver operating characteristic (ROC) curve shows that DNA methylation (show HELLS Antibodies) of COMT is able to predict the development of schizophrenia in males (area under curve [AUC]=0.802, P=1.91e-007).
COMT Met allele is associated with striatal gray matter volume alterations in Japanese children with ADHD.
Miroestrol restored uterine COMT expression in beta-naphthoflavone-treated mice.
This study report that genetically driven reduction in COMT enzyme activity increased cortical thickness in the prefrontal cortex (PFC (show CFP Antibodies)) and postero-parieto-temporal cortex of male, but not female adult mice.
COMT expression in the hippocampus was significantly reduced by high E2 replacement, implying increased catecholamine levels in the hippocampus of high E2 mice.
COMT overexpressing mice display an increase in dopamine release capacity in the striatum, suggesting increased COMT activity may affect dopamine signaling by enhancing synaptic clearance in the cortex and changes in striatal presynaptic dopamine function
These data confirm at the level of mouse working memory and human working memory-associated physiology a genetic interaction between COMT and DTNBP1 (show DTNBP1 Antibodies).
The results of this study suggest that individual differences in COMT activity do not affect primary reinforcing effects of cocaine in mice.
Inhibition of COMT via serotonin binding contributes to pain hypersensitivity.
COMT knockout mice were more impulsive compared with wild-type littermates.
Data show that in male catechol-O-methyltransferase COMT(-/-)-mice, the total number of T-, and B-lymphocytes from spleen increased but the T-cell proliferative response decreased.
decreased COMT activity was associated with some changes in feeding microstructure in rats and mice
An analysis of polymorphisms of the COMT gene as a preliminary step in evaluating the role of the gene in behavior is reported.
Catechol-O-methyltransferase catalyzes the transfer of a methyl group from S-adenosylmethionine to catecholamines, including the neurotransmitters dopamine, epinephrine, and norepinephrine. This O-methylation results in one of the major degradative pathways of the catecholamine transmitters. In addition to its role in the metabolism of endogenous substances, COMT is important in the metabolism of catechol drugs used in the treatment of hypertension, asthma, and Parkinson disease. COMT is found in two forms in tissues, a soluble form (S-COMT) and a membrane-bound form (MB-COMT). The differences between S-COMT and MB-COMT reside within the N-termini. Several transcript variants are formed through the use of alternative translation initiation sites and promoters.
, catechol-O-methyltransferase 1
, catechol O-methyltransferase, soluble form
, catechol O-methyltransferase, membrane-bound form