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anti-CNR1 antibody :: Rabbit CNR1 Polyclonal Antibody

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Catalog # MBS9606370
Unit / Price
  0.1 mL  /  $255 +1 FREE 8GB USB
  0.2 mL  /  $295 +1 FREE 8GB USB
Product Name

CNR1, Polyclonal Antibody

Popular Item
Full Product Name

CNR1 Antibody

Product Synonym Names
CANN6; Cannabinoid receptor 1; CB-R; CB1; CB1A; CB1K5; CB1R; Central cannabinoid receptor; CNR; CNR1; CNR1_HUMAN; OTTHUMP00000016838; OTTHUMP00000214579
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
3D Structure
ModBase 3D Structure for P21554
Clonality
Polyclonal
Isotype
IgG
Host
Rabbit
Species Reactivity
Human, Mouse, Rat
Specificity
CNR1 antibody detects endogenous levels of total CNR1
Purity/Purification
The antiserum was purified by peptide affinity chromatography using SulfoLink Coupling Resin.
Form/Format
Liquid
Phosphate buffered saline, pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Concentration
1mg/ml (lot specific)
Immunogen
A synthesized peptide
Subcellular Location
Cell Membrane
Tissue Specificity
Widely expressed, with highest levels in fetal and adult brain. Expression levels of isoform 2 and isoform 3 are much lower than those of isoform 1.
Conjugation
Unconjugated
Preparation and Storage
Store at -20 degree C. Stable for 12 months from date of receipt.
ISO Certification
Manufactured in an ISO 9001:2015 Certified Laboratory.
Supply Chain Verification
Manufactured in a lab with traceable raw materials manufactured on site. Coordinated product portfolio of antibodies, pairs, conjugates, recombinant proteins, and immunoassay materials available, please inquire.
Other Notes
Small volumes of anti-CNR1 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.
Related Product Information for
anti-CNR1 antibody
Function: 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).
Subunit Structure: Interacts (via C-terminus) with CNRIP1; this interaction attenuates constitutive, but not agonist-dependent, inhibition of voltage-gated Ca2+ channels in neurons (PubMed:17895407). Associates with G protein alpha subunits, including G(i) alpha-1/GNAI1, G(i) alpha-3/GNAI3 and G(o) alpha/GNAO1; palmitoylation is important for interaction with GNAI3 and GNAO1 (PubMed:12237474).
Post-translational Modifications: Palmitoylation at Cys-415 is important for recruitment at plasma membrane and lipid rafts and association with G protein alpha subunits.
Similarity: Belongs to the G-protein coupled receptor 1 family.
Applications Tested/Suitable for anti-CNR1 antibody
Western Blot (WB), Immunohistochemisty (IHC), Immunofluorescence (IF), Immunocytochemistry (ICC), ELISA (EIA)
Application Notes for anti-CNR1 antibody
WB: 1:500-1:1000
IHC: 1:50-1:200
IF/ICC: 1:100-1:500

Western Blot (WB) of anti-CNR1 antibody
Western blot analysis of extracts from COS-7cells using CNR1 antibody.The lane on the left is treated with the antigen-specific peptide.
anti-CNR1 antibody Western Blot (WB) (WB) image
Immunofluorescene (IF) of anti-CNR1 antibody
MBS9606370 staining 293T by IF/ICC. The sample were fixed with PFA and permeabilized in 0.1% Triton X-100, then blocked in 10% serum for 45 minutes at 25 degree C. The primary antibody was diluted at 1/200 and incubated with the sample for 1 hour at 37 degree C. An Alexa Fluor 594 conjugated goat anti-rabbit IgG (H+L) Ab, diluted at 1/600, was used as the secondary antibody.
anti-CNR1 antibody Immunofluorescene (IF) image
Immunohistochemistry (IHC) of anti-CNR1 antibody
MBS9606370 at 1/100 staining Human brain cancer tissue by IHC-P. The sample was formaldehyde fixed and a heat mediated antigen retrieval step in citrate buffer was performed. The sample was then blocked and incubated with the antibody for 1.5 hours at 22 degree C. An HRP conjugated goat anti-rabbit antibody was used as the secondary.
anti-CNR1 antibody Immunohistochemistry (IHC) (IHC) image
Western Blot (WB) of anti-CNR1 antibody
Western blot analysis of extracts from COS-7cells using CNR1 antibody.The lane on the left is treated with the antigen-specific peptide.
anti-CNR1 antibody Western Blot (WB) (WB) image
NCBI/Uniprot data below describe general gene information for CNR1. It may not necessarily be applicable to this product.
NCBI GI #
NCBI GeneID
NCBI Accession #
NCBI GenBank Nucleotide #
UniProt Primary Accession #
UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
Observed: 53 kD
Predicted: 53 kDa
NCBI Official Full Name
cannabinoid receptor 1 isoform a
NCBI Official Synonym Full Names
cannabinoid receptor 1
NCBI Official Symbol
NCBI Official Synonym Symbols
CB1; CNR; CB-R; CB1A; CB1R; CANN6; CB1K5
  [Similar Products]
NCBI Protein Information
cannabinoid receptor 1
UniProt Protein Name
Cannabinoid receptor 1
UniProt Synonym Protein Names
CANN6
Protein Family
UniProt Gene Name
UniProt Synonym Gene Names
CNR; CB-R; CB1  [Similar Products]
NCBI Summary for CNR1
This gene encodes one of two cannabinoid receptors. The cannabinoids, principally delta-9-tetrahydrocannabinol and synthetic analogs, are psychoactive ingredients of marijuana. The cannabinoid receptors are members of the guanine-nucleotide-binding protein (G-protein) coupled receptor family, which inhibit adenylate cyclase activity in a dose-dependent, stereoselective and pertussis toxin-sensitive manner. The two receptors have been found to be involved in the cannabinoid-induced CNS effects (including alterations in mood and cognition) experienced by users of marijuana. Multiple transcript variants encoding two different protein isoforms have been described for this gene. [provided by RefSeq, May 2009]
UniProt Comments for CNR1
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 (). 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 (). 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 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).
Precautions
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Disclaimer
While every efforts were made to ensure the accuracy of the information provided in this datasheet, MyBioSource will not be liable for any omissions or errors contained herein. MyBioSource reserves the right to make changes to this datasheet at any time without prior notice.

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