- Peptide (C)NGSKDGLDSNPMKD, corresponding to amino acid residues 11-24 of human CB2 receptor (Accession P34972). Extracellular, N-terminus.
- HL-60 (human promyelocytic leukaemia) and MCF-7 (human adenocarcinoma, mammary gland) cell line lysates (1:200).
- Western blot analysis of human HL-60 acute promyelocytic leukemia cell line lysate (lanes 1 and 2) and human MCF-7 breast adenocarcinoma cell line lysate (lanes 3 and 4):1,3. Anti-Human Cannabinoid Receptor 2 (extracellular) Antibody (#ACR-003), (1:200).
2,4. Anti-Human Cannabinoid Receptor 2 (extracellular) Antibody, preincubated with Human Cannabinoid Receptor 2 (extracellular) Blocking Peptide (#BLP-CR003).
- Human prostate cancer (LNCaP) live cells (1:50).
- Human promyelocytic leukaemia live cells (5 μg).
Cannabinoids have been used as pain relievers in Eastern medicine for many years.1 To date, two specific cannabinoid receptors have been identified: cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2).2 The cannabinoid receptors can be distinguished by their amino acid sequence, signaling mechanisms and tissue distribution.2 Both receptors belong to the G-protein coupled receptor superfamily and are coupled to Gi/0 G protein.2,3
The CB2 is highly expressed in cells of the immune system such as macrophages, lymphocytes natural killer cells and mast cells but has also been shown to be expressed, by both, in situ-hybridization and in immunohistochemistry, in spleen, thymus, and pancreas.1,2,4 CB2 expression in brain is still much less characterized than that of CB1. Recently, it was demonstrated that CB2 is expressed in the brain and might have a role in controlling fundamental processes such as proliferation and survival of neural cells.5,6
Overexpression of CB2 was reported in several cancers such as prostate, glioma and acute myeloid leukemias.7-9 In human astrocytoma a direct relation between CB2 expression and tumor malignancy was demonstrated.8 Activation of CB2R in vivo by its agonist JWH-133, completely blocked cell growth.8 In C6 glioma, it was shown that activation of the CB2 by JWH-133 resulted in internalization of only the CB2 and not CB1 leading to apoptosis of the cells. This may well be a new approach for the treatment of glioma.