Ask about this productRelated genes to: Gpr88 Blocking Peptide
- Gene:
- GPR88 NIH gene
- Name:
- G protein-coupled receptor 88
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-02
- Date modifiied:
- 2016-10-05
Related products to: Gpr88 Blocking Peptide
Related articles to: Gpr88 Blocking Peptide
- Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disease with high heterogeneity and currently lacks approved targeted therapies. Identifying druggable genes with diagnostic relevance and potential translational value may facilitate further research into precision medicine approaches for NAFLD. This study integrated transcriptome data from three independent GEO datasets (GSE33814, GSE63067, and GSE89632) and used sva and limma to correct for batch effects. Differentially expressed genes (DEGs), druggable genes obtained from DGIdb, and genes from WGCNA modules significantly associated with NAFLD were intersected to identify candidate genes. Candidate genes were systematically evaluated using functional enrichment analysis (GO, KEGG, GSEA), immune infiltration analysis (CIBERSORT), receiver operating characteristic (ROC) analysis, and co-expression networks. Finally, the expression of key genes was verified by immunohistochemistry (IHC) and immunofluorescence (IF). A total of nine key candidate drug targets were identified: FABP4, ADAMTS1, FOS, GPR88, IL1RL1, CD52, JUN, SERPINE1, and THBS1. These genes are primarily involved in metabolism, inflammatory response, extracellular matrix remodeling, and immune regulation. ROC analysis showed that FOS and JUN had high diagnostic accuracy. Furthermore, IHC and IF results demonstrated that CD52 was significantly upregulated in NAFLD tissues, suggesting its potential relevance as a candidate target for further investigation. This study systematically identified key druggable genes for NAFLD through bioinformatics analysis and partially validated selected candidates experimentally. In particular, CD52 was upregulated in NAFLD tissues, suggesting a potential association with NAFLD-related pathological alterations. These findings provide new insights into the molecular pathogenesis of NAFLD and may provide a basis for future target validation studies. - Source: PubMed
Publication date: 2026/05/20
Zhang XiangqianSu HanyangZhou QuanZhou Yuling - The peripheral nervous system retains the intrinsic ability to regenerate: after nerve injury, axons can sprout and reinnervate their target organ. We hypothesized that this regenerative response was driven by a transcriptional program involving druggable gene targets that promote neurite outgrowth. - Source: PubMed
Publication date: 2026/01/13
Ün DidemGilbert CatherineSteinkellner ThomasSalzer IsabellaFreissmuth Michael - From the approximately 800 members of the G protein-coupled receptor (GPCR) family, more than 100 remain orphans (oGPCRs). There is evidence indicating that some oGPCRs may carry out a physiological role independently from endogenous ligands; this includes forming heteromers with other GPCRs and altering their functional and pharmacological properties via allosteric interactions. Recent studies have shown that some of these oGPCRs, e.g. GPR88 and GPR139, allosterically inhibit opioid activity by interacting with the μ-opioid receptor (μOR). Here, we have focused on the characterization of the interaction between GPR88 and µOR and the allosteric mechanism of inhibition. We confirmed that GPR88 inhibits µOR function in striatal neuronal primary cultures. Moreover, using a peptide-interfering approach combined with biophysical and biochemical techniques, we identified that GPR88 and µOR interact via transmembrane helix 6. A combination of molecular dynamic simulations and site-directed mutagenesis have allowed to propose that the negative regulatory role of GPR88 on µOR is due to the Q298 side chain of GPR88. - Source: PubMed
Publication date: 2026/01/07
Llinas Del Torrent ClaudiaRaïch IuCarrasco-Martinez BertaLillo JaumeGallo MariaAndreu DavidPardo LeonardoNavarro Gemma - GPR88 is an orphan G protein-coupled receptor that regulates dopamine neurotransmission and is a target for neuropsychiatric disorders. In addition to the somatic membrane, GPR88 can localize to the primary cilium, a membrane microdomain known for dynamically enriching receptors and signaling molecules. However, the distribution of GPR88 in neuronal primary cilia remains uncharacterized. Here, we characterize GPR88 distribution at primary cilia in two brain areas. We show that in the striatum, GPR88 localizes both to somatodendritic and primary cilia compartments on inhibitory GABAergic medium spiny neurons. In contrast, in the somatosensory cortex, GPR88 localizes to somatodendritic and nuclear compartments and not primary cilia of excitatory spiny stellate neurons. In addition, we found that cilia density and length were similar between knockout and wild-type animals. Together, we provide key evidence for neuronal cell-type specific regulation of GPR88 localization to primary cilia, suggesting neuron subtype specific regulatory mechanisms govern receptor ciliary targeting in the brain. - Source: PubMed
Publication date: 2025/12/02
Li Guan Yenni HKieffer Brigitte Lvon Zastrow MarkEhrlich Aliza T - GPR88, an orphan G protein-coupled receptor primarily expressed in the striatum, has emerged as a potential target for treating alcohol use disorder (AUD) due to its role in modulating reward and motivational pathways. In this study, we investigated the effects of the GPR88 agonist RTI-122 on alcohol intake and motivation to self-administer alcohol under different conditions. In mice, RTI-122 reduced alcohol consumption in a two-bottle choice paradigm, which was prevented by Gpr88 knockout, confirming a GPR88-specific effect on the attenuation of alcohol drinking. In rats, RTI-122 dose-dependently reduced operant alcohol self-administration and decreased motivation to self-administer alcohol in progressive ratio tasks, regardless of whether the alcohol was adulterated with quinine or not. Additionally, a high dose of RTI-122 reduced yohimbine-induced reinstatement. Importantly, RTI-122 did not affect water intake in mice or sucrose self-administration in rats, indicating receptor- and reward-specific modulation of alcohol intake. These findings suggest that RTI-122, through GPR88 agonism, effectively reduces alcohol consumption and motivation across various contexts, positioning it as a promising lead for the development of new AUD treatments. - Source: PubMed
Lovelock Dennis FLiu WenHamida Sami BenCordero Victoria LVan Voorhies Kalynn JMartin MarionOlmo Isabella GuimaraesDarcq EmmanuelRahman Md ToufiqurNaassila MickaelKieffer Brigitte LJin ChunyangBesheer Joyce