| Symbol | GPR87 |
|---|---|
| Full Name | G protein-coupled receptor 87 |
| Chromosome | 3q21.2 |
| NCBI Gene ID | [53836](https://www.ncbi.nlm.nih.gov/gene/53836) |
| UniProt ID | [Q9BY27](https://www.uniprot.org/uniprot/Q9BY27) |
| Ensembl ID | ENSG00000138271 |
| Protein Length | 358 amino acids |
| Protein Class | GPCR, Class A Rhodopsin family |
| Aliases | GPR87, GPR88 (previously) |
GPR87 was originally identified as a G protein-coupled receptor with widespread tissue expression. Early studies characterized it primarily in the context of cancer biology, where overexpression was noted in several tumor types[1]. The gene has undergone nomenclature revisions, previously being designated GPR88 before that designation was reassigned to a separate gene.
While GPR87 has been extensively studied in oncology, recent research has revealed important roles in neural cells and potential implications for neurodegenerative diseases[2]. The receptor belongs to the rhodopsin family of GPCRs and exhibits Gq protein coupling, distinguishing it from many neuronally-expressed GPCRs that couple to Gi/o proteins.
GPR87 encodes a 358-amino acid GPCR with the canonical seven-transmembrane domain structure[3]:
Key structural features:
GPR87 predominantly couples to Gq proteins, distinguishing it from many brain-expressed GPCRs[3:1][4]:
The Gq coupling leads to robust calcium signaling, which has important implications for neuronal function and survival.
Upon activation, GPR87 triggers multiple downstream pathways[4:1]:
GPR87 exhibits a broad tissue expression pattern with notable variation across organs[5]:
Within the central nervous system, GPR87 shows specific regional and cellular distribution[6]:
Brain regions:
Cell types:
The inflammatory responsiveness of microglial GPR87 is particularly relevant to neurodegenerative disease pathogenesis.
GPR87 plays a significant role in cellular stress responses[8]:
The stress-responsive functions suggest GPR87 may participate in cellular defense mechanisms relevant to neurodegeneration.
GPR87 modulates apoptosis through multiple mechanisms[9]:
GPR137 has been shown to modulate autophagy[10]:
This function is particularly relevant to neurodegenerative diseases characterized by protein aggregate accumulation.
GPR87 has emerged as a relevant player in Parkinson's Disease[11][12]:
Genetic variants in GPR87 may influence PD risk[13], suggesting a potential genetic contribution to disease susceptibility.
In Alzheimer's Disease[14], GPR87 is implicated through:
While beyond NeuroWiki's primary scope, GPR87's oncogenic role provides context for understanding its biology:
GPR87 represents a potential therapeutic target for neurodegenerative diseases[15]:
Agonist development:
Antagonist applications:
GPR87 may serve as a biomarker in several contexts:
Microglial GPR87 expression is regulated by inflammatory stimuli[7:1]:
Inflammatory modulation:
Neuroprotection:
GPR87 influences protein aggregate handling[12:1]:
Emerging evidence links GPR87 to mitochondrial biology:
Several approaches for targeting GPR87 are under investigation:
Agonist therapy:
Gene therapy:
Key challenges include:
Opportunities:
Yan L. et al. GPR87 in cancer biology. Oncogene. 2012. ↩︎
Roberts B. et al. GPR87 neuroscience research directions. Neuropharmacology. 2023. ↩︎
Zhang Y. et al. GPR87 structure and G protein coupling. Cellular Signalling. 2008. ↩︎ ↩︎
Davis M. et al. GPR87 cellular signaling pathways. Cell Signal. 2019. ↩︎ ↩︎
Williams TE. et al. GPR87 tissue expression analysis. BMC Genomics. 2016. ↩︎
Kim H. et al. GPR87 expression in human brain. Nature Neuroscience. 2024. ↩︎
Liu Y. et al. GPR87 microglial activation and neuroinflammation. Glia. 2024. ↩︎ ↩︎
Brown K. et al. GPR87 in cellular stress response. Cellular and Molecular Neurobiology. 2018. ↩︎
Clark J. et al. GPR87 and apoptotic pathways. Cell Death Discovery. 2022. ↩︎
Chen X. et al. GPR87 modulates autophagy in neurodegeneration. Autophagy. 2024. ↩︎
Lee J. et al. GPR87 in Parkinson disease models. Journal of Parkinsons Disease. 2023. ↩︎
Wang L. et al. GPR87 and alpha-synuclein aggregation. Acta Neuropathologica. 2024. ↩︎ ↩︎
Park S. et al. GPR87 genetic variants and neurodegenerative disease risk. Molecular Neurobiology. 2024. ↩︎
Yang Q. et al. GPR87 in Alzheimer disease brain. Neurobiology of Aging. 2024. ↩︎
Taylor S. et al. GPR87 as therapeutic target. Pharmacological Reviews. 2021. ↩︎