Ask about this productRelated genes to: GPR37 antibody
- Gene:
- GPR37 NIH gene
- Name:
- G protein-coupled receptor 37
- Previous symbol:
- -
- Synonyms:
- EDNRBL, hET(B)R-LP, PAELR
- Chromosome:
- 7q31.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-12
- Date modifiied:
- 2017-05-02
Related products to: GPR37 antibody
Related articles to: GPR37 antibody
- Chronic stress significantly impacts hippocampal function through transcriptional and epigenetic mechanisms. While the roles of lncRNAs in stress-related transcriptional and epigenetic regulation have recently been recognized, their genome-wide functions controlling the transcriptional network remain largely unclear. Evidence indicates that the lncRNA uc.104 is involved in stress responses; however, its genome-wide chromatin interactions and gene regulatory effects are yet to be explored. To examine this, we combined chromatin isolation by RNA purification sequencing (ChIRP-seq) and RNA sequencing (RNA-seq) in the hippocampus from handled control and chronic restraint stress (CRS) rats. ChIRP-seq identified 6,664 uc.104 binding peaks under CRS, including 6,517 enriched and 149 reduced. Many peaks were mapped to intronic and promoter-proximal regions of protein-coding genes. Integration of ChIRP-seq with RNA-seq data revealed 1,839 differentially expressed genes associated with uc.104 binding sites, with 106 high-confidence overlaps. Several genes (Gabra3, Htr7, Irs1, Gpr37, Clu, Hspa1b, Ppp3r2, Nfasc, Pcdhac2, and Cysltr2) identified as regulatory targets of uc.104, have been directly implicated in stress responses, synaptic plasticity, and neuroinflammation. Gene ontology and Synapse GO (SynGO) analyses revealed significant enrichment for processes involving dendritic spine formation, synapse organization, and pre- and postsynaptic signaling. Protein-protein interaction analysis identified hub genes, including EGFR, CDC42, IGF1R, CTNNB1, CALM1, CALM3, POLR2A, MDM2, TBP, and CSNK1E, several of which have been linked to stress-responsive pathways. Together, our findings reveal that uc.104 binding to chromatin near stress- and synapse-related genes may act as a regulator of stress-responsive transcriptional networks in the hippocampus. By linking uc.104 occupancy to stress and synaptic responsive genes, this study highlights uc.104 as a potential mediator of stress-induced hippocampal malfunctions. - Source: PubMed
Publication date: 2026/04/19
Verma Anuj KRoy BhaskarPrall KevinHulwi EllieDwivedi Yogesh - - Source: PubMed
Publication date: 2026/04/18
Liu XuemeiWang ShuaiyuLai JuanGao XiangWang LinaFeng BoYang LiangQian ZhengjiangJiang RuotianChu JunTan LimingLi XiangWang Liping - , an ancient cnidarian, exhibits remarkable regenerative and neurogenic abilities, mediated by morphogenetic peptides, particularly the head activator peptide. This neuropeptide appears to regulate cell proliferation, differentiation, and nerve net maintenance in hydra and, surprisingly, exerts similar mitogenic and neurogenic effects in mammalian systems. Despite early enthusiasm, research on head activator has declined, due to controversies about its genetic origin, receptor identity, and artefacts generated during isolation. Nonetheless, a synthetic variant of head activator corresponding to the described sequence has consistently exhibited strong biological activity in a variety of mammalian cells. Experimental evidence implicates the sortilin-related receptor (SorLA) as a primary receptor in mammals, with potential modulatory roles for the G-protein-coupled receptor GPR37. This review consolidates current knowledge on the evolutionary context, molecular characteristics, and functional activities of head activator. Insights from mammalian systems highlight its pleiotropic effects across species. Given its neuroprotective, regenerative, and immunomodulatory properties, head activator may merit reconsideration as a therapeutic candidate for neurodegenerative disorders and regenerative medicine. - Source: PubMed
Publication date: 2026/03/30
Klymenko AndriiLutz David - G protein-coupled receptor 37 (GPR37) and G protein-coupled receptor 37 like 1 (GPR37L1) are implicated in tumorigenesis; however, their prognostic significance and roles in chemotherapy and immunotherapy responses across diverse cancers is incompletely defined. Utilizing transcriptomic, genomic, pharmacogenomic, and clinical data, we mapped the molecular landscapes of GPR37 and GPR37L1 and assessed their potential clinical value in retrospective real-world cohorts. Our analysis revealed high genetic alteration rates for GPR37 (10.2%) and GPR37L1 (10.7%). Aberrant expression of GPR37 served as a predictive biomarker for survival outcomes in breast invasive carcinoma, lower grade gliomas, and lung adenocarcinoma, a pattern similarly observed for GPR37L1. Intriguingly, the 2 receptors exhibited divergent prognostic effects in adrenocortical carcinoma, cervical squamous cell carcinoma and endocervical adenocarcinoma, lung squamous cell carcinoma, stomach adenocarcinoma, uterine corpus endometrial carcinoma, and uveal melanoma. Evaluation of chemotherapy response identified significant correlations between the expression levels of both GPR37 and GPR37L1 and sensitivity to 21 common chemotherapeutic agents. For example, in lung adenocarcinoma, the elevated expression of either receptor was significantly associated with reduced sensitivity to cisplatin and gemcitabine. Analysis of 2 immunotherapy-treated melanoma cohorts demonstrated that high GPR37 or GPR37L1 expression correlated with inferior overall survival, a finding corroborated by immune infiltration and chemokine profiles. Our in vitro experiments demonstrated that the proposed ligand TX14A was unable to activate GPR37 and GPR37L1 through the cyclic adenosine monophosphate or extracellular signal-regulated kinase/mitogen-activated protein kinase pathways. Notably, this is the first systematic pan-cancer profiling of both GPR37 and GPR37L1 that integrates analyses of chemotherapy sensitivity, immunotherapy response, and immune landscapes. GPR37 and GPR37L1 may represent candidate biomarkers for prognostic stratification and for predicting chemotherapy and immunotherapy response. - Source: PubMed
Zhu GuoqiangHe JiliangShi NingkunCai ZhongyaoZhang JiannanWang Susanna Chau YiLi JuanZhang MaoWang Yajun - Rapid escape from visual threats is essential for survival, yet the mechanisms establishing its "permissive state" remain poorly understood. Here, we demonstrate that osteocalcin (OCN), a bone-derived hormone, permits rapid visual escape by enhancing the excitability of a ventral tegmental area (VTA) GABAergic neuron subpopulation through the OCN-G Protein-Coupled Receptor 37 (GPR37)-cAMP-TWIK-related halothane-inhibited potassium channel (THIK-1) pathway. Loss of OCN, loss of its receptor GPR37, or conditional deletion of GPR37 in VTA GABAergic or glutamatergic neurons delays escape responses, while reconstituting OCN-GPR37 signaling in the VTA restores normal behavior. Single-cell transcriptomics and electrophysiology reveal that OCN suppresses THIK-1 potassium currents via GPR37-mediated cyclic AMP (cAMP) reduction, thereby increasing neuronal excitability. These findings reveal a novel mechanism through which a bone-derived hormone modulates the excitability of co-releasing neurons to facilitate rapid escape, offering new insights into the regulation of survival behaviors by the bone-brain metabolic axis. - Source: PubMed
Publication date: 2026/02/11
Liu XuemeiWang ShuaiyuLai JuanGao XiangWang LinaFeng BoYang LiangQian ZhengjiangJiang RuotianChu JunTan LimingLi XiangWang Liping