Ask about this productRelated genes to: GPRC5B Blocking Peptide
- Gene:
- GPRC5B NIH gene
- Name:
- G protein-coupled receptor class C group 5 member B
- Previous symbol:
- -
- Synonyms:
- RAIG-2
- Chromosome:
- 16p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-11
- Date modifiied:
- 2016-10-06
Related products to: GPRC5B Blocking Peptide
Related articles to: GPRC5B Blocking Peptide
- Despite its strong regenerative capacity, liver aging paradoxically increases susceptibility to fibrosis and metabolic dysfunction-associated steatotic liver disease through dysregulated inflammation, senescence-associated secretory phenotypes, and immune-metabolic crosstalk. To systematically characterize these processes, we integrated longitudinal transcriptomics, single-cell RNA sequencing, and machine-learning approaches. We identified 252 aging-associated genes and developed an Aging Gene Score (AGS) to quantify senescence burden across hepatic cell populations. Single-cell analysis revealed macrophages as key drivers of fibrosis progression, with high-AGS myeloid subsets markedly expanded in cirrhotic livers. Using combined Boruta and LASSO algorithms, we established a five-gene biomarker panel (EFEMP1, LUM, DKK3, GPRC5B, NCAM2) that accurately predicts advanced fibrosis (AUC > 0.77). Furthermore, a network pharmacology framework was applied to screen medicine-food homology (MFH) herbs, identifying Fagopyrum dibotrys (Jinqiaomai) and Astragalus membranaceus (Huangqi) as top candidates. Molecular docking demonstrated strong binding between the bioactive compound MOL000098 and the fibrosis-related target COL3A1. Functional assays showed that Jinqiaomai-containing serum alleviates oxidative stress, improves HepG2 cell viability, reduces ALT and AST levels, and suppresses macrophage lipid accumulation, accompanied by reduced expression of inflammatory and fibrosis-related markers. Collectively, our findings highlight macrophage-centered mechanisms linking liver aging and fibrosis and suggest MFH-derived compounds as promising anti-aging and anti-fibrotic dietary interventions. - Source: PubMed
Publication date: 2026/05/26
Xu YingqiLi MaohaoZhu LunLuo YawenSheng WanluJia PanleiSuo RinaBao Lidao - Osteosarcoma, the most common primary malignant bone tumor with poor prognosis, underscores the need for a deeper understanding of its molecular mechanisms. Recent studies have highlighted the importance of RNA modifications, including 5-methylcytosine (m5C), in cancer progression, yet the m5C modification landscape in osteosarcoma remains unexplored. Here, we performed transcriptome-wide profiling of m5C modifications in osteosarcoma using meRIP-seq and RNA-seq, analyzing four pairs of osteosarcoma and adjacent normal tissues. Furthermore, through conjunction analyses of meRIP-seq and RNA-seq data, we identified 637 genes with significant changes in both the m5C modification and mRNA levels. Among these, GPRC5B emerged as a key prognostic gene, with its high expression and m5C hypermethylation significantly associated with poor survival in osteosarcoma patients. Functional experiments demonstrated that GPRC5B suppresses apoptosis and promotes osteosarcoma cell proliferation and migration. Mechanistically, NSUN2-mediated m5C modification upregulates GPRC5B expression, and the anti-apoptotic effects of NSUN2 are primarily dependent on its ability to modulate GPRC5B m5C modification and expression. Knockdown of GPRC5B partially rescues the anti-apoptotic effects of NSUN2, highlighting the critical role of GPRC5B in osteosarcoma survival. Our study identified an m5C-dependent NSUN2-GPRC5B regulatory axis, providing insights into osteosarcoma progression and revealing its therapeutic potential. - Source: PubMed
Publication date: 2026/03/18
Chen ZhenyiYang MinLiang XiaoxiaoYang ZhiqiangMai WulanWang YuyangLu YushenWang RuiminHan YuanhangXie YuanlongCai Lin - Metabolic syndrome (MetS) is a recognized risk factor for prostate cancer (PCa), yet the precise biological mechanisms driving this association remain poorly understood. Unraveling these molecular pathways is essential for developing targeted interventions to improve patient outcomes. In this study, we analyzed NHANES (2005-2014) data to examine associations between MetS and PCa outcomes, finding that MetS was significantly associated with higher PCa risk (OR = 1.52), all-cause mortality (HR = 1.53), and cancer-specific mortality (HR = 2.17). Through integrated multi-omics, weighted gene co-expression network analysis, and machine learning, we identified the orphan receptor GPRC5B as a critical hub gene downregulated in both conditions. Single-cell transcriptomic analysis further confirmed that GPRC5B is predominantly expressed in endothelial cells. Mechanistically, GPRC5B loss was found to hyperactivate p38 MAPK signaling through a specific dual mechanism: increasing phosphorylation of upstream MKK3/6 kinases while concurrently suppressing the negative feedback phosphatase DUSP1. This synergistic dysregulation drove enhanced endothelial proliferation, migration, and tube formation in vitro. In vivo, endothelial GPRC5B deficiency significantly accelerated tumor growth and neovascularization, phenotypes that were effectively reversed by the p38 inhibitor SB202190. Clinical specimens corroborated reduced GPRC5B expression and increased microvessel density in MetS-associated PCa. Collectively, our findings establish endothelial GPRC5B downregulation as a key molecular driver promoting pathological angiogenesis via the MKK3/6-DUSP1-p38 axis, suggesting that targeting this signaling cascade offers a promising therapeutic strategy for managing MetS-associated PCa aggression. - Source: PubMed
Publication date: 2026/02/22
Lin WeilongChen PeixianOu YuanHuang ShanheLi ZonglinHuang JinxingWang BaojunXie RuihuiHuang Hai - Volume-regulated anion channels (VRACs) are central to cell volume homeostasis. They mediate swelling-induced efflux of chloride and organic osmolytes to drive regulatory volume decrease. In the brain, VRACs have been proposed to play a key role in astrocytic volume regulation. Genetic defects in astrocytic VRAC modulating proteins (MLC1, GlialCAM, Aquaporin-4, GPRC5B) cause the leukodystrophy Megalencephalic leukoencephalopathy with subcortical cysts (MLC), characterized by chronic white matter edema and myelin vacuolization. Disrupted VRAC activity in MLC-patient-derived lymphoblasts and primary astrocytes from MLC mice further supports a pathogenic link between defective VRAC activity and MLC. Here, we studied the physiological and pathological consequences of astrocyte-specific removal of the essential VRAC subunit LRRC8A. In contrast to established MLC mouse models, astrocyte specific Lrrc8a knockout mice had normal brain water content, no myelin vacuolization, and preserved expression of MLC-related proteins. At a late age they developed a mildly ataxic gait and displayed increased severity of kainate-induced seizures. Two-photon imaging in acute brain slices revealed that astrocytes lacking LRRC8A show normal volume recovery and chloride dynamics upon high potassium-induced cell swelling. Together, these findings demonstrate that astrocyte LRRC8A is not essential for volume regulation in situ and that its loss alone is insufficient to cause the chronic white matter edema typical of MLC. The mild neurological deficits indicate a physiological role for astrocyte LRRC8A, but MLC pathology likely arises from broader dysregulation of the astrocytic protein complex coordinating ion and water homeostasis. - Source: PubMed
Publication date: 2026/02/05
Kerst SvenHoogterp LeoniBreur Marjoleinvan Rooijen-van Leeuwen Gemma MBugiani MariannaSah RajanMansvelder Huibert Dvan der Knaap Marjo SMin Rogier - The paper is aimed to screen the target molecules of miR-12 and to further explore the mechanism of GAS5 action in prostate cancer. The expression of GPRC5B in prostate cancer cell lines LNCaP, VCaP, 22RV1, DU145, and PC3 was measured by quantitative real-time PCR with reverse transcription (RT-qPCR) and variations in GPRC5B expression were analyzed after down-regulating GAS5 or silencing miR-12. CCK8 and plate clone experiments were performed to detect changes in proliferative activity and colony-forming capacity of prostate cancer cells after down-regulating GPRC5B. After transfection of prostate cancer cells with sh-GAS5 and/or miR-12 inhibitor, the changes in GPRC5B expression were evaluated with RT-qPCR and Western blotting. Our results showed that GPRC5B was highly expressed in prostate cancer cell lines. Down-regulating of GAS5 decreased GPRC5B expression, while silencing miR-12 increased it. CCK8 and plate clone experiments showed that expression of GPRC5B increased proliferative activity and clone formation ability of prostate cancer cells. RT-qPCR and Western blotting revealed that miR-12 inhibited the promoting effect of GAS5 on GPRC5B expression. Thus, GPRC5B is directly bound to miR-12. GAS5 promotes proliferation, migration, and invasion of prostate cancer cells and participates in malignant progression of tumors by suppressing miR-12-mediated regulation of GPRC5B expression. - Source: PubMed
Publication date: 2026/01/08
Li Cang