Human COMT blocking peptide

Name: Human COMT blocking peptide
SKU: CDBP0850
Rating: 5 (1 reviews)

Synthetic Human COMT blocking peptide for Apuri, BL, ELISA

COA

SDS

Datasheet

Summary

Product Overview

Blocking/Immunizing peptide for anti-COMT (internal) antibody

Target

COMT (internal)

Nature

Synthetic

Tag/Conjugate

Unconjugated

Application Notes

For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not for human or animal consumption.

Format

Lyophilized powder

Preservative

None

Storage

Shipped at ambient temperature, store at -20°C.

Entrez Gene ID

1312

Antigen Description

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.

Function

O-methyltransferase activity; catechol O-methyltransferase activity; magnesium ion binding; transferase activity;

Synonyms

COMT; catechol-O-methyltransferase; catechol O-methyltransferase;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Child psychiatry interventions in patients with 22q11 deletion syndrome: From treatment to prevention

ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE

Authors: Novo, A.; Woestelandt, L.; Rousselot-Pailley, B.; Leitgel, M.; Eutrope, J.; Rio, M.; Lyonnet, S.; Robel, L.

Abstract

22q11.2DS is one of the more frequent genetic syndromes associated to psychiatric symptoms. It has been associated to an increased risk to develop schizophrenia in adolescence or early adulthood. However, psychiatric symptoms appear early on, and should be recognized as soon as possible by child psychiatrists in order to improve the present well-being of children and their family, and to prevent further risks of developing severe and chronic psychiatric diseases later on. In this paper, we present a review of the recent literature concerning the 22q11.2DS syndrome focused on the risk factors that may be associated to an increased risk of psychotic transition. We advocate for the development of systematic specialized child psychiatry consultations for these patients, included in networks with geneticists, adult psychiatrists, and family associations, in order to improve their psychiatric prognosis and to support the development of translational research. (C) 2018 L'Encephale, Paris.

Genetic variation of cisplatin-induced ototoxicity in non-cranial-irradiated pediatric patients using a candidate gene approach: The International PanCareLIFE Study

PHARMACOGENOMICS JOURNAL

Authors: Clemens, Eva; Broer, Linda; Langer, Thorsten; Uitterlinden, Andre G.; de Vries, Andrica C. H.; van Grotel, Martine; Pluijm, Saskia F. M.; Binder, Harald; Byrne, Julianne; Broeder, Eline van Dulmen-den; Crocco, Marco; Grabow, Desiree; Kaatsch, Peter; Kaiser, Melanie; Kenborg, Line; Winther, Jeanette F.; Rechnitzer, Catherine; Hasle, Henrik; Kepak, Tomas; van der Kooi, Anne-Lotte F.; Kremer, Leontien C.; Kruseova, Jarmila; Kuehni, Claudia E.; van der Pal, Heleen; Parfitt, Ross; Deuster, Dirk; Matulat, Peter; Spix, Claudia; Tillmanns, Amelie; Tissing, Wim J. E.; Maier, Lara; Zehnhoff-Dinnesen, Antoinette; Zolk, Oliver; van den Heuvel-eibrink, Marry M.

Abstract

Ototoxicity is a common side effect of platinum treatment and manifests as irreversible, high-frequency sensorineural hearing loss. Genetic association studies have suggested a role for SNPs in genes related to the disposition of cisplatin or deafness. In this study, 429 pediatric patients that were treated with cisplatin were genotyped for 10 candidate SNPs. Logistic regression analyses revealed that younger age at treatment (<= 5 years vs >15 years: OR: 9.1; 95% CI: 3.8-21.5; P = 5.6 x 10(-7)) and higher cumulative dose of cisplatin (>450 vs <= 300 mg/m(2): OR: 2.4; 95% CI: 1.3-4.6; P = 0.007) confer a significant risk of ototoxicity. Of the SNPs investigated, none of them were significantly associated with an increase of ototoxicity. In the meta-analysis, ACYP2 rs1872328 (OR: 3.94; 95% CI: 1.04-14.03; P = 0.04) and SLC22A2 rs316019 (OR: 1.46; 95% CI: 1.07-2.00; P = 0.02) were associated with ototoxicity. In order to increase the understanding of the association between SNPs and ototoxicity, we propose a polygenic model, which takes into account multiple interacting genes of the cisplatin pathway that together confer an increased risk of ototoxicity.