| TAAR2 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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| Aliases | TAAR2, GPR58, taR-2, trace amine associated receptor 2, trace amine associated receptor 2 (gene/pseudogene) | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM:604849;MGI:2685071;HomoloGene:110760;GeneCards:TAAR2;OMA:TAAR2 - orthologs | ||||||||||||||||||||||||||||||||||||||||||||||||||
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| Wikidata | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Trace amine-associated receptor 2 (TAAR2), formerly known asG protein-coupled receptor 58 (GPR58), is aprotein that in humans is encoded by theTAAR2gene.[5][6][7][8] TAAR2 is co-expressed withGα proteins;[8] however, as of February 2017,[update] itssignal transduction mechanisms have not been determined.[8]
Human TAAR2 (hTAAR2) is expressed in thecerebellum,olfactory sensory neurons in theolfactory epithelium, andleukocytes (i.e., white blood cells), among other tissues.[9][10]hTAAR1 and hTAAR2 are both required for white blood cell activation bytrace amines ingranulocytes.[11]
Using brain histochemistry staining of mice with LacZ insertion into TAAR2 gene histochemical reaction was found in the glomerular layer of theolfactory bulb, but intensive staining was found in the deeper layer as well. The histochemical reaction was observed in the fibers of theolfactory nerve, in the glomeruli of the glomerular layer, several short axon (SA) cells (outer plexiform layer or granular layer) and neuronal projections that were visualized throughout the depth of the olfactory bulb. Furthermore, LacZ staining was observed in the limbic areas of the brain receiving olfactory input, i.e.,piriform cortex molecular area,hippocampus (CA1 field, pyramidal layer),hypothalamic lateral zone (zone incerta) and lateralhabenula. In addition, a histochemical reaction was found in the midbrainraphe nuclei and primarysomatosensory area of thecortex (layer 5). Real-time quantitative PCR with reverse transcription confirmed TAAR2 gene expression in the mouse brain areas such as thefrontal cortex,hypothalamus, andbrainstem.[12][13]
TAAR2knockout mice have significantly higher level ofdopamine in thestriatum tissue than wild-type littermates and lower level ofnorepinephrine inhippocampus. Also, they have lower levels ofMAO-B expression inmidbrain andstriatum. A significantly higher number of thedopamine neurons was detected in TAAR2-KO mice in thesubstantia nigrapars compacta. TAAR2 knockout mice have significantly higher level of horizontal activity and lower immobilization time inforced swim test.[12]
It has been found that TAAR2 knockout mice have an increased number of neuroblast-like and proliferating cells in both subventricular and subgranular zones of thedentate gyrus in comparison to wild type animals. Furthermore, TAAR2 knockout mice have an increased thebrain-derived neurotrophic factor (BDNF) level in thestriatum.[12]
Asingle nucleotide polymorphismnonsense mutation of the TAAR2 gene is associated withschizophrenia.[8][9] TAAR2 is a probablepseudogene in 10–15% of Asians as a result of apolymorphism that produces apremature stop codon at amino acid 168.[8]
TCells, B Cells and Peripheral Mononuclear cells express TAAR2 mRNA. Migration toward TAAR1 ligands required both TAAR1 and TAAR2 expression based on siRNA experiments.[11] In T cells, the same stimuli triggered cytokine secretion while in B cells Immunoglobulin secretion is triggered.[11]
3‐Iodothyronamine (T1AM) was identified as anon-selective ligand for TAAR2.[10] Additional TAAR1 ligands,tyramine andphenethylamine trigger TAAR2 dependant actions, though direct binding has not been demonstrated.[11]
This article incorporates text from theUnited States National Library of Medicine, which is in thepublic domain.
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