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AB5636P

Sigma-Aldrich

Anti-Cannabinoid Receptor 1 Antibody, NT

Chemicon®, from rabbit

Synonyme(s) :

CB1

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

100

Forme d'anticorps

affinity purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

polyclonal

Produit purifié par

affinity chromatography

Espèces réactives

human, rat, mouse

Fabricant/nom de marque

Chemicon®

Technique(s)

ELISA: suitable
western blot: suitable

Numéro d'accès NCBI

NM_016083.3
NM_033181.2

Numéro d'accès UniProt

P21554

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... CNR1(1268)
mouse ... Cnr1(12801)

Spécificité

Recognizes human Cannabinoid Receptor 1 (CB1). The immunogen shows no significant sequence homology with CB2 or other receptors.

Immunogène

A 14 amino acid N-terminus peptide sequence (aa 1-14) (Gerard et al. 1991; Gerard et al.

1990; Shire et al. 1995; Matsuda et al. 1990; Ho et al. 1996; Chakraborty et al. 1995).
Epitope: N-terminus

Application

Research Category
Neuroscience
Research Sub Category
Neuroinflammation & Pain

Neurotransmitters & Receptors
This Anti-Cannabinoid Receptor 1 Antibody, N-terminus is validated for use in ELISA, WB for the detection of Cannabinoid Receptor 1.
Western blot: 1-10 μg/mL using ECL. Expected sizes are ~60kDa and 80-84kDa under reducing conditions.

ELISA: 1:10,000-1:100,000 using 50-100 ng control peptide (Cat. No. AG357) per well.

Optimal working dilutions must be determined by the end user.

Description de la cible

~60kDa and 80-84kDa

Forme physique

Affinity Purified immunoglobulin. Liquid in 100mM Tris, pH 7.5, containing 0.2% BSA and 0.05% sodium azide.
ImmunoAffinity Purified

Stockage et stabilité

Maintain for 1 year at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Remarque sur l'analyse

Control
Brain tissue

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Informations légales

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 2

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Cannabinoid control of brain bioenergetics: Exploring the subcellular localization of the CB1 receptor.
Hebert-Chatelain, E; Reguero, L; Puente, N; Lutz, B; Chaouloff, F; Rossignol, R; Piazza et al.
Molecular Metabolism null
C Song et al.
Life sciences, 56(23-24), 1983-1989 (1995-01-01)
To study the N-linked glycosylation properties of the CB1 receptor, rat brain membranes were treated with exo- and endoglycosidases. For visualizing CB1 receptors, an antipeptide antibody was raised against the N-terminal 14 amino acids and used to specifically detect the
Andrew P Ray et al.
Behavioural brain research, 196(1), 30-36 (2008-08-30)
Cisplatin chemotherapy frequently causes severe vomiting in two temporally separated clusters of bouts dubbed the acute and delayed phases. Cannabinoids can inhibit the acute phase, albeit through a poorly understood mechanism. We examined the substrates of cannabinoid-mediated inhibition of both

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