• Rat CNR1 (Cannabinoid Receptor 1, Brain) Sandwich ELISA Kit (STJE0008010)

Rat CNR1 (Cannabinoid Receptor 1, Brain) Sandwich ELISA Kit (STJE0008010)

SKU:
STJE0008010

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Applications: ELISA
Reactivity: Rat
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Sensitivity: 0.056ng/mL
Detection Limit: 0.156-10ng/mL
Short Description: This CNR1 Sandwich ELISA Kit is an in-vitro enzyme-linked immunosorbent assay for the measurement of samples in rat cell culture supernatant, serum and plasma (EDTA, citrate, heparin).
Storage Instruction: Store the unopened kit in the fridge at 2-8°C for up to 6 months. Once opened store individual kit contents according to components table provided with the kit.
Assay Time: 4.5 hrs
Gene Symbol: Cnr1
Gene ID: 25248
Uniprot ID: CNR1_RAT
Sample Type: tissue homogenates, cell lysates or other biological fluids.
Tissue Specificity Expressed in the brain, in the striatum, medial septum, descending arm of the band of Broca, the amygdaloid nucleus, the hippocampus and cortex (at protein level). High levels in the lateral striatum. In rostral brain regions, high expression levels in the dorsal lateral striatum, while in the caudal brain regions, high levels are observed in the ventral lateral striatum. Expressed in monocytes/macrophages (at protein level). Expressed in striated muscles and in vascular smooth muscles cells (at protein level).
Post Translational Modifications Palmitoylation at Cys-416 is important for recruitment at both plasma membrane and lipid rafts and association with G protein alpha subunits.
Function G-protein coupled receptor for cannabinoids, including endocannabinoids (eCBs), such as N-arachidonoylethanolamide (also called anandamide or AEA) and 2-arachidonoylglycerol (2-AG). 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 Ca(2+) 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. In response to cannabinoid anandamide, elicits a pro-inflammatory 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.
Protein Name Cannabinoid Receptor 1
Cb-R
Cb1
Brain-Type Cannabinoid Receptor
Database Links Reactome: R-RNO-373076
Reactome: -RNO-418594
Cellular Localisation Cell Membrane
Multi-Pass Membrane Protein
Mitochondrion Outer Membrane
Cell Projection
Axon
Presynapse
Unexpectedly
In The Mitochondria
The C-Terminus Is Located In The Mitochondrial Intermembrane Space
A Compartment Topologically Considered As Extracellular
In Canonical Seven-Transmembrane G-Protein Coupled Receptors
The C-Terminus Is Cytosolic
In Interneurons
Found On The Membrane Of Cytoplasmic Compartments
Some Of Which Could Be Elements Of The Endosome-Lysosome System And Multivesicular Bodies
Found On Presynaptic Axon Terminals In Some Gabaergic Neurons In The Somatosensory Cortex
Alternative ELISA Names Cannabinoid Receptor 1 ELISA kit
Cb-R ELISA kit
Cb1 ELISA kit
Brain-Type Cannabinoid Receptor ELISA kit
Cnr1 ELISA kit
Skr6 ELISA kit
output

Information sourced from Uniprot.org

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