CNR1 antibody (N-Term)

Catalog No. ABIN6257095

This anti-CNR1 antibody is a Rabbit Polyclonal antibody detecting CNR1 in WB, ELISA, IHC, ICC and IF. Suitable for Human, Rat and Mouse.

Quick Overview for CNR1 antibody (N-Term) (ABIN6257095)

Target: CNR1 (Cannabinoid Receptor 1 (CNR1))

Reactivity: Human, Rat, Mouse

Host: Rabbit

Clonality: Polyclonal

Conjugate: This CNR1 antibody is un-conjugated

Application: Western Blotting (WB), ELISA, Immunohistochemistry (IHC), Immunocytochemistry (ICC), Immunofluorescence (IF)

Product Details anti-CNR1 Antibody

Binding Specificity: N-Term

Specificity: CNR1 Antibody detects endogenous levels of total CNR1.

Predicted Reactivity: Bovine,Horse,Sheep,Chicken

Purification: The antiserum was purified by peptide affinity chromatography using SulfoLink^TM Coupling Resin (Thermo Fisher Scientific).

Immunogen: A synthesized peptide derived from human CNR1, corresponding to a region within N-terminal amino acids.

Isotype: IgG

Application Details

Application Notes: WB 1:500-1:1000, IHC: 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000

Restrictions: For Research Use only

Handling

Format: Liquid

Concentration: 1 mg/mL

Buffer: Rabbit IgG in phosphate buffered saline , pH 7.4, 150 mM NaCl, 0.02 % sodium azide and 50 % 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

Storage Comment: Store at -20 °C. Stable for 12 months from date of receipt.

Expiry Date: 12 months

Target Details for CNR1

Target: CNR1 (Cannabinoid Receptor 1 (CNR1))

Alternative Name: CNR1

Background:

Description: G-protein coupled receptor for endogenous cannabinoids (eCBs), including N-arachidonoylethanolamide (also called anandamide or AEA) and 2-arachidonoylglycerol (2-AG), as well as phytocannabinoids, such as delta9-tetrahydrocannabinol (THC) (PubMed:15620723, PubMed:27768894, PubMed:27851727). 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 (PubMed:1718258, PubMed:21895628, PubMed:27768894). 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 (By similarity). In superior cervical ganglions and cerebral vascular smooth muscle cells, inhibits voltage-gated Ca2+ channels in a constitutive, as well as agonist-dependent manner (PubMed:17895407). In cerebral vascular smooth muscle cells, cannabinoid-induced inhibition of voltage-gated Ca2+ channels leads to vasodilation and decreased vascular tone (By similarity). 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 (By similarity). 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 (By similarity). 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 (By similarity). In response to cannabinoid anandamide, elicits a proinflammatory response in macrophages, which involves NLRP3 inflammasome activation and IL1B and IL18 secretion (By similarity). 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).

Gene: CNR1

Molecular Weight: 53 kDa

Gene ID: 1268

UniProt: P21554

Pathways: Feeding Behaviour