Cannabinoid receptor 1 (CNR1), rat, recombinant

Organism: Rattus norvegicus (Rat). Source: in vitro E.coli expression system. Expression Region: 1-473aa. Protein Length: Full Length. Tag Info: N-terminal 10xHis-tagged. Target Protein Sequence: MKSILDGLAD TTFRTITTDL LYVGSNDIQY EDIKGDMASK LGYFPQKFPL TSFRGSPFQE KMTAGDNSPL VPAGDTTNIT EFYNKSLSSF KENEENIQCG ENFMDMECFM ILNPSQQLAI AVLSLTLGTF TVLENLLVLC VILHSRSLRC RPSYHFIGSL AVADLLGSVI FVYSFVDFHV FHRKDSPNVF LFKLGGVTAS FTASVGSLFL TAIDRYISIH RPLAYKRIVT RPKAVVAFCL MWTIAIVIAV LPLLGWNCKK LQSVCSDIFP LIDETYLMFW IGVTSVLLLF IVYAYMYILW KAHSHAVRMI QRGTQKSIII HTSEDGKVQV TRPDQARMDI RLAKTLVLIL VVLIICWGPL LAIMVYDVFG KMNKLIKTVF AFCSMLCLLN STVNPIIYAL RSKDLRHAFR SMFPSCEGTA QPLDNSMGDS DCLHKHANNT ASMHRAAESC IKSTVKIAKV TMSVSTDTSA EAL. Purity: Greater than 90% as determined by SDS-PAGE. Endotoxin: Not test. Biological Activity: n/a. Form: Liquid or Lyophilized powder. Buffer: If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0. Reconstitution: We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20 °C/-80 °C. Our default final concentration of glycerol is 50%. Customers could use it as reference. Storage: The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. Generally, the shelf life of liquid form is 6 months at -20 °C/-80 °C. The shelf life of lyophilized form is 12 months at -20 °C/-80 °C. Notes: Repeated freezing and thawing is not recommended. Store working aliquots at 4 °C for up to one week. Relevance: 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 . Reference: "Activation of the Nlrp3 inflammasome in infiltrating macrophages by endocannabinoids mediates beta cell loss in type 2 diabetes." Jourdan T., Godlewski G., Cinar R., Bertola A., Szanda G., Liu J., Tam J., Han T., Mukhopadhyay B., Skarulis M.C., Ju C., Aouadi M., Czech M.P., Kunos G. Nat. Med. 19:1132-1140(2013). Function: nan