GPR156
GPR156 | |||
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Identifiers | |||
Gene ontology | |||
Molecular function | |||
Cellular component | |||
Biological process | |||
Sources:Amigo / QuickGO |
Ensembl | |||||||||
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UniProt | |||||||||
RefSeq (mRNA) | |||||||||
RefSeq (protein) | |||||||||
Location (UCSC) | Chr 3: 120.16 – 120.29 Mb | Chr 16: 37.74 – 37.83 Mb | |||||||
PubMed search | [3] | [4] |
View/Edit Human | View/Edit Mouse |
GPR156 (G protein-coupled receptor 156), is a human gene which encodes a G protein-coupled receptor belonging to metabotropic glutamate receptor subfamily.[5] By sequence homology, this gene was proposed as being a possible GABAB receptor subunit, however when expressed in cells alone or with other GABAB subunits, no response to GABAB ligands could be detected. In vitro studies on GPR156 constitutive activity revealed a high level of basal activation and coupling with members of the Gi/Go heterotrimeric G protein family.[6] In 2021, an article was reported that GPR156 modulates hair cell orientation in the cochlea.[7] Also, it was proposed that GPR156 is related to congenital hearing loss.[8] GPR156 in complex with any of the Gi/o heterotrimers regulates the hair cell orientation.[9] In 2024, molecular structures of G-free and Go-bound GPR156 were characterized by using cryogenic electron microscopy.[10]
Structure
Among class C GPCR family members, GPR156 is unique because it lacks a large extracellular domain. Structural analyses revealed that the asymmetric binding of Go-protein to GPR156 triggers conformational change of its cytoplasmic face without altering dimer interface.[10] Although the inactive class C GPCRs undergo rearrangement of their dimeric interface, the agonist- and/or the positive allosteric modulator-bound class C GPCRs retain their dimeric interface upon G-protein binding. Thus, the G-free GPR156 is likely to represent an active state.[10] Structural and functional analyses suggest that abundant endogenous phospholipids, receptor dimerization, and the G-protein binding-induced conformational change of the cytoplasmic face are the primary reasons for constitutive activation of GPR156.[10] Phosphatidylglycerol further stimulates the activity of GPR156, which suggests the environmental changes of the phospholipid composition may regulate the GPR156 activity.[10]
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000175697 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000046961 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Entrez Gene: GPR156 G protein-coupled receptor 156".
- S2CID 232430996.
- PMID 34001891.
- PMID 37814107.
- .
- ^ PMID 38332368.
Further reading
- Calver AR, Michalovich D, Testa TT, Robbins MJ, Jaillard C, Hill J, Szekeres PG, Charles KJ, Jourdain S, Holbrook JD, Boyfield I, Patel N, Medhurst AD, Pangalos MN (2003). "Molecular cloning and characterisation of a novel GABAB-related G-protein coupled receptor". Brain Res. Mol. Brain Res. 110 (2): 305–17. PMID 12591167.
- Vassilatis DK, Hohmann JG, Zeng H, Li F, Ranchalis JE, Mortrud MT, Brown A, Rodriguez SS, Weller JR, Wright AC, Bergmann JE, Gaitanaris GA (2003). "The G protein-coupled receptor repertoires of human and mouse". Proc. Natl. Acad. Sci. U.S.A. 100 (8): 4903–8. PMID 12679517.