Rat CNR1/Cannabinoid Receptor 1 ELISA Kit | CNR1 elisa kit

Rat CNR1/Cannabinoid Receptor 1 ELISA Kit

Cat. Num. AAA2890326

• Gene Names: Cnr1; SKR6R
• Reactivity: Rat
• Synonyms: CNR1/Cannabinoid Receptor 1; Rat CNR1/Cannabinoid Receptor 1 ELISA Kit; Cannabinoid receptor 1; Brain-type cannabinoid receptor; Skr6; CNR1 elisa kit

• Reactivity: Rat
• Specificity: Natural and recombinant Rat Cannabinoid receptor 1
• Sequence Length: 473

• Assay Type: Sandwich
• Detection Range: 78-5000pg/mL
• Sensitivity: 24pg/mL
• Preparation and Storage: For long term storage, please store the entire kit at -20 degree C.

Typical Testing Data/Standard Curve (for reference only)

NCBI and Uniprot Product Information

• NCBI GI #: 6978673
• NCBI GeneID: 25248
• NCBI Accession #: NP_036916.1
• NCBI GenBank Nucleotide #: NM_012784.5
• 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).