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cannabinoid receptor 1
Human cannabinoid receptor 1 (CB1) bound to tetrahydrocannabinol agonist AM11542 (black). PDB: 5XRA
Identifiers
Symbol
CNR1
Alt. symbols
CNR
NCBI gene
1268
HGNC
2159
OMIM
114610
Orthologs
7273
RefSeq
NM_033181
UniProt
P21554
Other data
Locus
Chr. 6 q14-q15
Search for
Structures
Swiss-model
Domains
InterPro
cannabinoid receptor 2
Human cannabinoid receptor 2 (CB2) bound to agonist AM10257 (black). PDB: 5ZTY
Identifiers
Symbol
CNR2
NCBI gene
1269
HGNC
2160
OMIM
605051
Orthologs
1389
RefSeq
NM_001841
UniProt
P34972
Other data
Locus
Chr. 1 p
Search for
Structures
Swiss-model
Domains
InterPro
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Cannabinoid receptors, located throughout the body, are part of the endocannabinoid system of vertebrates– a class of cell membrane receptors in the G protein-coupled receptor superfamily.[1][2][3][4] As is typical of G protein-coupled receptors, the cannabinoid receptors contain seven transmembrane spanning domains.[5] Cannabinoid receptors are activated by three major groups of ligands:
Endocannabinoids;
Phytocannabinoids (plant-derived such as tetrahydrocannabinol (THC) produced by cannabis);
Synthetic cannabinoids (such as HU-210).
All endocannabinoids and phytocannabinoids are lipophilic.
There are two known subtypes of cannabinoid receptors, termed CB1 and CB2.[6][7] The CB1 receptor is expressed mainly in the brain (central nervous system or "CNS"), but also in the lungs, liver and kidneys. The CB2 receptor is expressed mainly in the immune system, in hematopoietic cells,[8] and in parts of the brain.[9]
The protein sequences of CB1 and CB2 receptors are about 44% similar.[10][11] When only the transmembrane regions of the receptors are considered, amino acid similarity between the two receptor subtypes is approximately 68%.[5] In addition, minor variations in each receptor have been identified. Cannabinoids bind reversibly and stereo-selectively to the cannabinoid receptors. Subtype selective cannabinoids have been developed which theoretically may have advantages for treatment of certain diseases such as obesity.[12]
Enzymes involved in biosynthesis/inactivation of endocannabinoids and endocannabinoid signaling in general (involving targets other than CB1/2-type receptors) occur throughout the animal kingdom.[13]
^Cite error: The named reference pmid12432948 was invoked but never defined (see the help page).
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^Aizpurua-Olaizola O, Elezgarai I, Rico-Barrio I, Zarandona I, Etxebarria N, Usobiaga A (January 2017). "Targeting the endocannabinoid system: future therapeutic strategies". Drug Discovery Today. 22 (1): 105–110. doi:10.1016/j.drudis.2016.08.005. PMID 27554802. S2CID 3460960. Archived from the original on 2023-01-27. Retrieved 2022-10-19.
^ abCite error: The named reference pmid7556170 was invoked but never defined (see the help page).
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^Pacher P, Mechoulam R (April 2011). "Is lipid signaling through cannabinoid 2 receptors part of a protective system?". Progress in Lipid Research. 50 (2): 193–211. doi:10.1016/j.plipres.2011.01.001. PMC 3062638. PMID 21295074.
^Jordan CJ, Xi ZX (March 2019). "Progress in brain cannabinoid CB2 receptor research: From genes to behavior". Neuroscience and Biobehavioral Reviews. 98: 208–220. doi:10.1016/j.neubiorev.2018.12.026. PMC 6401261. PMID 30611802.
^Latek D, Kolinski M, Ghoshdastider U, Debinski A, Bombolewski R, Plazinska A, et al. (September 2011). "Modeling of ligand binding to G protein coupled receptors: cannabinoid CB1, CB2 and adrenergic β 2 AR". Journal of Molecular Modeling. 17 (9): 2353–66. doi:10.1007/s00894-011-0986-7. PMID 21365223. S2CID 28365397.
^Cite error: The named reference pmid7689702 was invoked but never defined (see the help page).
^Kyrou I, Valsamakis G, Tsigos C (November 2006). "The endocannabinoid system as a target for the treatment of visceral obesity and metabolic syndrome". Annals of the New York Academy of Sciences. 1083 (1): 270–305. Bibcode:2006NYASA1083..270K. doi:10.1196/annals.1367.024. PMID 17148745. S2CID 23486551.
^Elphick MR (December 2012). "The evolution and comparative neurobiology of endocannabinoid signalling". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 367 (1607): 3201–15. doi:10.1098/rstb.2011.0394. PMC 3481536. PMID 23108540.
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