- 貨號 Cat. No.
- ACR-001
- 規格 Size
- 50 μl 0.2ml
Description
Anti-Cannabinoid Receptor 1 (extracellular)
Epitope: |
Peptide NKSLSSFKENEENIQC corresponding to amino acid residues 84-99 of rat CB1 receptor (Accession P20272). |
Putative epitope location: |
Extracellular, N-Terminus |
Homology: |
Human ?identical; Mouse ?15/16 amino acid residues identical. |
Reactivity Confirmed: |
Rat, mouse. |
Applications:
 |
Western blot analysis of rat brain membrane proteins:
1. Anti-CB1R (extracellular) antibody (#ACR-001) (1:200).
2. Anti-CB1R(extracellular) antibody preincubated with the control peptide antigen. |
Immunohistochemistry: |
Expression of CB1R in mouse hippocampus |
 |
Immunohistochemical staining of cannabinoid receptor 1 (CB1R) in mouse hippocampus using Anti-CB1R (extracellular) antibody (#ACR-001) (1:100). (A) CB1R was detected in pyramidal and infra-pyramidal layers (green). (B) Staining of interneurons using mouse anti-parvalbumin (PV) antibody (red). (C) Confocal merge of Anti-CB1R (extracellular) and anti-PV antibody stainings does not indicate the presence of CB1R in GABAergic cells. |
 |
Immunohistochemical staining of cannabinoid receptor 1 (CB1R) in rat hippocampus using Anti-CB1R (extracellular) antibody (#ACR-001) (1:100). (A) CB1R was detected in pyramidal and infra-pyramidal layers (green). (B) Staining of interneurons using mouse anti-parvalbumin (PV) antibody (red). (C) Confocal merge of Anti-CB1R (extracellular) and anti-PV antibody stainings does not indicate the presence of CB1R in GABAergic cells. |
1. Brooks, J.W. and Fraquhar-Smith, M.A. (2003) Br. J. Anaesth. 3, 175. |
2. Howlett, A.C. (2002) Prostaglandins Other Lipid Mediat. 68?9, 619. |
3. Howlett, A.C. et al. (2002) Pharmacol. Rev. 54,161. |
4. Rueda, D. et al. (2000) Mol. Pharmacol. 58, 814. |
5. Sarfaraz, S. et al. (2005) Cancer Res. 65, 1635. |
6. Casanova, M.L. et al. (2003) J. Clin. Invest. 111, 43. |
7. Cota, D. et al. (2003) Int. J. Obes. Relat. Metab. Disord. 27, 289. |
Cannabinoids have been used in Eastern medicine for many years as pain relievers.1 D9-tetrahydrocannabinol (THC), the major psychoactive compound in marijuana and hashish, has been shown to interact with two specific cannabinoid receptors: cannabinoid receptor 1 (CB1 Receptor or CB1R) and cannabinoid receptor 2 (CB2 Receptor or CB2R).2 The cannabinoid receptors can be distinguished by their amino acid sequences, signaling mechanisms, and tissue distributions.2 Both receptors belong to the G-protein-coupled receptor (GPCR) superfamily. CB1R was shown to modulate several Ca2+ and K+ ion channels.2,3
CB1R is primarily expressed in the central nervous system. However, expression of CB1R is also detected in the peripheral terminals, in non-neuronal peripheral tissues such as uterus, testes, spleen, as well as in cells of the immune system.3,4
CB1R is implicated in many cellular functions such as neurotransmitter release, pain relief, cancer, and obesity.5,6 Growth inhibition of tumor cells was demonstrated following mixed CB1R/CB2R agonist treatment in both prostate and non-melanoma skin cancers.5,6 Through their interaction with CB1R, cannabinoid compounds stimulate appetite for sweets and palatable foods in particular, making CB1R an attractive therapeutic target for the treatment of obesity and eating disorders.7
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