Catechol-O-Methyltransferase (COMT) (AA 26-141) antibody

Details for Product No. ABIN968704
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Synonyms COMT, mb-comt, s-comt, comt, MGC154444, Comt1, D16Wsu103e, D330014B15Rik
AA 26-141
(42), (25), (17), (17), (11), (10), (5), (5), (4), (2), (2), (1), (1), (1), (1), (1), (1)
Mouse (Murine)
(181), (40), (38), (7), (3), (2), (2), (1)
(129), (61), (26), (1)
Clonality (Clone)
Monoclonal ()
(12), (12), (12), (9), (9), (9), (1), (1), (1), (1), (1), (1), (1), (1)
Western Blotting (WB), Immunofluorescence (IF)
(174), (120), (59), (32), (32), (12), (10), (8), (7), (5), (4), (4), (3), (2), (1)
Pubmed 3 references available
Quantity 50 μg
Shipping to United States (Change)
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Catalog No. ABIN968704
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Immunogen Mouse COMT
Clone 4
Isotype IgG1
Cross-Reactivity Rat (Rattus)
Characteristics 1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
4. Source of all serum proteins is from USDA inspected abattoirs located in the United States.
Purification Purified from tissue culture supernatant or ascites by affinity chromatography.
Alternative Name COMT
Background Catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) are the major mammalian enzymes involved in the degradation of the catecholamine neurotransmitters, dopamine, norepinephrine, and epinephrine. COMT is a Mg2+-dependent enzyme that catalyzes the transfer of methyl groups from S-adenosyl methionine to a hydroxyl group of a catecholic substrate. Two forms of COMT are found in rat brain, a 24 kDa soluble COMT (S-COMT) and a 28 kDa membrane-bound COMT (MB-COMT). COMT is widely expressed in brain, but its importance in catecholamine neurotransmitter degradation relative to MAO varies in different brain regions. In addition, COMT may function primarily in extraneuronal areas, such as in glial cells and postsynaptic neurons. COMT-deficient mice have sex- and region-specific alterations in dopamine levels in the brain, and display impaired emotional reactivity and aggressive behavior. Thus, COMT-mediated degradation of catecholamines in the brain may have important roles in maintaining normal catecholamine levels, as well as normal social behavior. This antibody is routinely tested by western blot analysis.
Synonyms: Catechol-O-Methyltransferase
Molecular Weight 24/28 kDa
Research Area Signaling, Metabolism

Related Products: ABIN967389

Restrictions For Research Use only
Format Liquid
Concentration 250 µg/ml
Buffer Aqueous buffered solution containing BSA, glycerol.
Preservative Sodium azide
Precaution of Use This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage -20 °C
Supplier Images
anti-Catechol-O-Methyltransferase (COMT) (AA 26-141) antibody Western blot analysis of COMT on a rat pituitary lysate. Lane 1: 1:10,000, lane 2: 1:20,000, lane 3: 1:40,000 dilution of the anti- COMT antibody.
anti-Catechol-O-Methyltransferase (COMT) (AA 26-141) antibody (2) Immunofluorescence staining of rat cortical neurons.
Product cited in: Werner, Di Rocco, Prikhojan et al.: "COMT-dependent protection of dopaminergic neurons by methionine, dimethionine and S-adenosylmethionine (SAM) against L-dopa toxicity in vitro." in: Brain research, Vol. 893, Issue 1-2, pp. 278-81, 2001 (PubMed).

Gogos, Morgan, Luine et al.: "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, Vol. 95, Issue 17, pp. 9991-6, 1998 (PubMed).

Tilgmann, Melen, Lundström et al.: "Expression of recombinant soluble and membrane-bound catechol O-methyltransferase in eukaryotic cells and identification of the respective enzymes in rat brain." in: European journal of biochemistry / FEBS, Vol. 207, Issue 2, pp. 813-21, 1992 (PubMed).

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