Ask about this productRelated genes to: GPR174 Blocking Peptide
- Gene:
- GPR174 NIH gene
- Name:
- G protein-coupled receptor 174
- Previous symbol:
- -
- Synonyms:
- FKSG79
- Chromosome:
- Xq21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-02
- Date modifiied:
- 2016-10-05
Related products to: GPR174 Blocking Peptide
Related articles to: GPR174 Blocking Peptide
- GPR174 is an immune-restricted G-protein-coupled receptor (GPCR) constitutively activated by lysophosphatidylserine (LysoPS). Elevated LysoPS in the tumor microenvironment may sustain GPR174 activity, promoting immunosuppression and resistance to cancer immunotherapies. Here, we modeled GPR174 bound to an antagonist mPS (modified LysoPS) and performed extensive molecular dynamics (MD) simulations in a heterogeneous lipid bilayer, with parallel simulations of the LysoPS-bound receptor for comparison. mPS binding inactivated GPR174 and resulted in reduced conformational dynamics, persistent hydrogen bonding interactions, and selective interactions with transmembrane helix 1. In contrast, LysoPS exhibited greater conformational flexibility, multiple binding poses, and transient acyl chain displacement into the membrane. Network analysis revealed that LysoPS engaged conserved activation motifs (PIF, DRY, N/DPxxY) to couple the ligand binding site to the G-protein interface, whereas these pathways were disrupted by mPS. Protein-lipid analyses further suggested that membrane lipids, including phosphatidylinositol (PIP2), modulate ligand dynamics and receptor conformational states. Collectively, these findings highlight distinct ligand-specific mechanisms of GPR174 modulation and provide a framework for rational design of selective antagonists with immunotherapeutic potential. - Source: PubMed
Publication date: 2025/09/19
Bhardwaj Vijay KumarGorfe Alemayehu - Autoimmune diseases are characterized by a dysfunction of the immune system. Disruptions in the balance of B-cell dynamics and the increase in auto-antibody levels are pivotal in the triggering of several autoimmune disorders. All of this is inextricably linked to the differentiation, development, migration, and functional regulation of B cells in the human immune response. G protein-coupled receptors (GPCR) are recognized as crucial targets in drug development and play pivotal roles in both B cell differentiation and the underlying mechanisms of autoimmune diseases. However, there has been an inadequate comprehension of how GPCR intricately modulate B cell development and impact the pathogenesis of autoimmune diseases. Ligands and functions of GPCR-chemokine receptors including CXCR3, CXCR4, CXCR5 and CCR7, lipid receptors including S1PR1-5, cannabinoid receptor CB2 as well as orphan GPCR including GPR132, GPR183, GPR174, and P2RY8 in B cell differentiation and development, will be elaborated in this review. The roles these GPCR play in mediating B cells in several autoimmune diseases will also be discussed. The elucidation of the multifaceted mechanisms controlled by GPCR not only enriches our comprehension of immune responses but also provides a promising avenue for therapeutic interventions in the domain of autoimmune disorders. - Source: PubMed
Publication date: 2025/04/30
Shao YongqiMei YangTan YixinYang MingWu Haijing - Esophageal squamous cell carcinoma (ESCC) is a highly lethal malignancy with a 5-year survival rate of less than 20%, largely due to its high propensity for metastasis and recurrence. There is an urgent need to identify targeted therapeutic agents for this disease. While lysophosphatidylserine (LysoPS) and its receptor GPR174 are known regulators of immune and inflammatory processes, their mechanistic role in ESCC progression remains unexplored. This study investigates the LysoPS/GPR174 axis in driving ESCC metastasis and its underlying molecular pathways. - Source: PubMed
Publication date: 2025/04/14
Xiao RongXu PeiLi XiangyuanShen FengTao ShuangfenZhu XiaocenCai YuFeng ZhuoweiLiu ZhiyiXiao HaiboDing FangbaoZhu Meiling - Glioblastoma (GBM) is the most common malignant brain tumor with poor overall survival. Current treatment management for GBM has low efficacy, mainly due to high inter-patient heterogeneity. The transcription profiles in GBM define cell properties essential for tumor progression. We have developed an approach for the identification of master regulators (MRs) that are responsible for the gene expression changes in GBM. The approach is based on transcription factor enrichment analysis with subsequent "upstream" analysis in the signaling network. The main feature of the approach is that all calculations are performed for transcription profiles from individual samples, which allows taking into account GBM transcription heterogeneity. We identified 451 MRs that were up-regulated or down-regulated and, thus, were important parts of positive feedback loops. The number of MRs in the samples correlated with the degree of tumor immune infiltration, while the differences in MR profiles were generally consistent with the known GBM subtypes: mesenchymal, classical, and proneural. MRs densely interact with each other in the signaling network that may be associated with the robustness to pharmacological intervention. We identified 102 receptors among MRs, which is coherent with the importance of cell-cell interactions for GBM progression. The role of some of them in GBM is not currently investigated: lysophosphatidic acid receptors 5 and 6, sphingosine-1-phosphate receptor 4, lysophosphatidylserine receptors GPR34 and GPR174, and G protein-coupled receptors 84 and 132 for fatty acids. Information on the revealed MRs can be used to search for novel therapeutic strategies to treat GBM. - Source: PubMed
Publication date: 2024/09/28
Ivanov Sergey MLagunin Alexey ATarasova Olga A - Although metagenomic investigations into microbial fiber-degrading capabilities are currently prevalent, there is a notable gap in research concerning the regulatory mechanisms underpinning host-microbiota interactions that confer tolerance to high-fiber diets in pigs. In this study, 28 Meishan (MS) and 28 Large White (LW) pigs were subjected to feeding experiments involving various fiber levels. Subsequently, multi-omics was employed to investigate the influence of host-microbiota interactions on the fiber degradation of pigs. MS exhibited superior fiber digestibility compared with LW, particularly evident when fed a high-fiber diet. In MS, positive interactions among , sp., bacterium, and bacterium WCE2004 facilitated the degradation of both cellulose and pectin. The reduced polymerization of polysaccharides and oligosaccharides observed in MS provides compelling evidence for their superior microbial fiber-degrading capability. The concentrations of propionate and butyrate retained in cecal lumen of MS was unchanged, whereas it was significantly increased in LW, indicating a strong absorption of short-chain fatty acids (SCFAs) in MS intestines. Correlation analysis using RNA-seq data revealed distinct patterns in LW and MS. In LW, microbial profiles along with and exhibited negative correlations with butyrate and propionate, respectively. Conversely, in MS, and were positively correlated with butyrate. Our findings underscore the dynamic collaboration among microbial species in degrading cellulose and pectin, coupled with the synergistic effects of SCFA transport-related genes, as crucial underpinnings for the heightened fiber digestibility observed in MS. These discoveries offer fresh perspectives into the intricate mechanisms governing host-microbiota interactions that influence fiber digestion in pigs. - Source: PubMed
Publication date: 2025/01/28
Pu GuangHou LimingZhao QingboLiu GenshengWang ZhongyuZhou WuduoNiu PeipeiWu ChengwuLi PinghuaHuang Ruihua