Rabbit anti-Mouse, Rat Cannabinoid Receptor 1 Polyclonal Antibody | anti-Cnr1 antibody

Anti-Cannabinoid Receptor 1 (Extracellular) Antibody

Cat. Num. AAA4157630

• Gene Names: Cnr1; SKR6R
• Reactivity: Mouse, Rat
• Applications: Western Blot, Immunohistochemistry
• Purity: Affinity Purified On Immobilized Antigen.
• Synonyms: Cannabinoid Receptor 1; Polyclonal Antibody; Anti-Cannabinoid Receptor 1 (Extracellular) Antibody; anti-Cnr1 antibody

• Host: Rabbit
• Reactivity: Mouse, Rat
• Clonality: Polyclonal
• Isotype: IgG
• Purity/Purification: Affinity Purified On Immobilized Antigen.
• Form/Format: Liquid; PBS, pH 7.4 with 0.05% sodium azide.
• Concentration: 1ug/ul (varies by lot)
• Sequence Length: 473

• Applicable Applications for anti-Cnr1 antibody: Western Blot (WB), Immunohistochemistry (IHC)
• Immunogen: Peptide NKSLSSFKENEENIQC corresponding to amino acid residues 84-99 of rat CB1 receptor (Accession P20272).
• Preparation and Storage: This product is stable for several weeks at 4 degree C as an undiluted liquid. Dilute only prior to immediate use.; For extended storage, aliquot contents and freeze at-20 degree C or below. Avoid cycles of freezing and thawing. Expiration date is one (1) year from date of receipt.

Testing Data

Testing Data

Testing Data

Related Product Information for anti-Cnr1 antibody

Cannabinoids have been used in Eastern medicine for many years as pain relievers.1 D9-tetrahydrocannabinol (THC), the major psychoactive compound in marijuana and hashish, has been shown to interact with two specific cannabinoid receptors: cannabinoid receptor 1 (CB1 Receptor or CB1R) and cannabinoid receptor 2 (CB2 Receptor or CB2R).2 The cannabinoid receptors can be distinguished by their amino acid sequences, signaling mechanisms, and tissue distributions.2 Both receptors belong to the G-protein-coupled receptor (GPCR) superfamily. CB1R was shown to modulate several Ca2+ and K+ ion channels.2, 3 CB1R is primarily expressed in the central nervous system. However, expression of CB1R is also detected in the peripheral terminals, in non-neuronal peripheral tissues such as uterus, testes, spleen, as well as in cells of the immune system.3, 4 CB1R is implicated in many cellular functions such as neurotransmitter release, pain relief, cancer, and obesity.5, 6 Growth inhibition of tumor cells was demonstrated following mixed CB1R/CB2R agonist treatment in both prostate and non-melanoma skin cancers.5, 6 Through their interaction with CB1R, cannabinoid compounds stimulate appetite for sweets and palatable foods in particular, making CB1R an attractive therapeutic target for the treatment of obesity and eating disorders.7

NCBI and Uniprot Product Information

• NCBI GI #: 6978673
• NCBI GeneID: 25248
• NCBI GenBank Nucleotide #: NP_036916.1
• UniProt Accession #: P20272
• NCBI Official Full Name: cannabinoid receptor 1
• NCBI Official Synonym Full Names: cannabinoid receptor 1
• NCBI Official Symbol: Cnr1
• NCBI Official Synonym Symbols: SKR6R
• NCBI Protein Information: cannabinoid receptor 1
• UniProt Protein Name: Cannabinoid receptor 1
• Protein Family: Cannabinoid receptor
• UniProt Gene Name: Cnr1
• UniProt Synonym Gene Names: CB-R; CB1

NCBI Description

G-protein coupled receptor for psychoactive cannabinoids; may mediate inhibition of NO production and participate in retrograde signaling by endocannabinoids [RGD, Feb 2006]

Uniprot Description

G-protein coupled receptor for cannabinoids, including endocannabinoids (eCBs), such as N-arachidonoylethanolamide (also called anandamide or AEA) and 2-arachidonoylglycerol (2-AG) (PubMed:2165569). Mediates many cannabinoid-induced effects, acting, among others, on food intake, memory loss, gastrointestinal motility, catalepsy, ambulatory activity, anxiety, chronic pain. Signaling typically involves reduction in cyclic AMP. In the hypothalamus, may have a dual effect on mitochondrial respiration depending upon the agonist dose and possibly upon the cell type. Increases respiration at low doses, while decreases respiration at high doses. At high doses, CNR1 signal transduction involves G-protein alpha-i protein activation and subsequent inhibition of mitochondrial soluble adenylate cyclase, decrease in cyclic AMP concentration, inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system, including NDUFS2. In the hypothalamus, inhibits leptin-induced reactive oxygen species (ROS) formation and mediates cannabinoid-induced increase in SREBF1 and FASN gene expression. In response to cannabinoids, drives the release of orexigenic beta-endorphin, but not that of melanocyte-stimulating hormone alpha/alpha-MSH, from hypothalamic POMC neurons, hence promoting food intake. In the hippocampus, regulates cellular respiration and energy production in response to cannabinoids. Involved in cannabinoid-dependent depolarization-induced suppression of inhibition (DSI), a process in which depolarization of CA1 postsynaptic pyramidal neurons mobilizes eCBs, which retrogradely activate presynaptic CB1 receptors, transiently decreasing GABAergic inhibitory neurotransmission. Also reduces excitatory synaptic transmission (). In superior cervical ganglions and cerebral vascular smooth muscle cells, inhibits voltage-gated Ca2+ channels in a constitutive, as well as agonist-dependent manner (). Induces leptin production in adipocytes and reduces LRP2-mediated leptin clearance in the kidney, hence participating in hyperleptinemia. In adipose tissue, CNR1 signaling leads to increased expression of SREBF1, ACACA and FASN genes. In the liver, activation by endocannabinoids leads to increased de novo lipogenesis and reduced fatty acid catabolism, associated with increased expression of SREBF1/SREBP-1, GCK, ACACA, ACACB and FASN genes. May also affect de novo cholesterol synthesis and HDL-cholesteryl ether uptake (). Peripherally modulates energy metabolism. In high carbohydrate diet-induced obesity, may decrease the expression of mitochondrial dihydrolipoyl dehydrogenase/DLD in striated muscles, as well as that of selected glucose/ pyruvate metabolic enzymes, hence affecting energy expenditure through mitochondrial metabolism (PubMed:26671069). In response to cannabinoid anandamide, elicits a proinflammatory response in macrophages, which involves NLRP3 inflammasome activation and IL1B and IL18 secretion. In macrophages infiltrating pancreatic islets, this process may participate in the progression of type-2 diabetes and associated loss of pancreatic beta-cells (PubMed:23955712).