Ask about this productRelated genes to: NRBP1 Blocking Peptide
- Gene:
- NRBP1 NIH gene
- Name:
- nuclear receptor binding protein 1
- Previous symbol:
- NRBP
- Synonyms:
- BCON3, MUDPNP, MADM
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-18
- Date modifiied:
- 2016-10-05
Related products to: NRBP1 Blocking Peptide
Related articles to: NRBP1 Blocking Peptide
- Recent studies have linked modifiable risk factors (RFs) to melanoma, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC). This study aimed to investigate the causal relationships between 11 modifiable RFs and these skin cancers and to identify novel therapeutic targets using multi-omics approaches. - Source: PubMed
Publication date: 2026/07/07
Qin ZhenHuoshen WudaLi XueqingLi ShiyuSun ChenYi Sha - Alcohol dependence currently lacks targeted pharmacotherapies, underscoring the urgent need for novel therapeutic targets. Existing research on disease-associated DNA methylation changes and their gene regulatory effects remains inconsistent. To resolve this uncertainty, we applied the Mendelian randomization to elucidate causal mechanisms connecting druggable genes, epigenetic regulation and alcohol dependence development. Integrating MR, colocalization and mediation analyses, we leveraged genome-wide association study (GWAS) (FinnGen), eQTL (eQTLGen) and methylation (GoDMC) data. We assessed causal gene-alcohol dependence relationships, shared causal variants via colocalization and methylation-mediated regulatory mechanisms. Our integrative analysis identified 10 drug-targetable genes showing significant expression alterations in alcohol dependence (FDR < 0.05), with three genes (CDK5R1, CAMKK2 and NRBP1) demonstrating evidence of shared causal variants through colocalization. Epigenetic regulation was particularly evident at two methylation sites (cg07437263 and cg05102552) that indirectly influenced alcohol dependence risk by modulating CDK5R1 (63.92% mediation) and NRBP1 (95.12% mediation) expression. These findings reveal DNA methylation as a critical regulatory mechanism governing neuronal gene expression patterns in alcohol dependence pathogenesis. The strong mediation effects observed for CDK5R1 and NRBP1, coupled with their colocalization evidence, position these genes as promising candidates for both biomarker development and targeted therapeutic interventions in alcohol dependence. This investigation spotlights the regulatory function of DNA methylation on CDK5R1 and NRBP1 in alcohol dependence. It implies that CDK5R1 and NRBP1 could serve as potential clinical biomarkers or therapeutic targets for the early management of alcohol dependence. - Source: PubMed
Deng FuyuanPeng JunshengLai SiranZhang GuangpengLi MiaomiaoHuang YuxinYuan MiYao GaoleiZhang PeimingLu Liming - Gestational diabetes mellitus (GDM) is a prevalent metabolic disorder during pregnancy associated with adverse maternal and fetal outcomes, highlighting the urgent need for novel, genetically supported drug targets due to suboptimal glycemic control and safety concerns with existing therapies. This study integrated cis-expression quantitative trait loci (cis-eQTL) of druggable genes with genome-wide association data to identify putative causal genes for GDM through two-sample Mendelian randomization (MR), with significant associations further validated using multi-tissue summary data-based Mendelian randomization (SMR), colocalization analysis, cis-protein quantitative trait loci (cis-pQTL) MR, and single-cell RNA sequencing (scRNA-seq) to confirm tissue- and cell type specific expression. MR analysis identified 15 genes significantly associated with GDM risk after Bonferroni correction, with SMR and colocalization analyses confirming robust associations for five key genes: higher expression of NRBP1, LPL, and BTN3A2 was causally linked to reduced GDM risk, while elevated GSTM1 and GRINA levels were associated with increased risk. ScRNA-seq revealed distinct expression patterns in placental cell types, with NRBP1 and GRINA highly expressed in trophoblasts and certain immune cell populations. Phenome-wide association studies revealed no significant pleiotropic effects, and pharmacological drug-target databases identified several compounds with potential regulatory interactions. This multi-omics study successfully identifies several genetically supported, druggable targets for GDM, providing a robust foundation for developing mechanism-based therapeutics and precision prevention strategies in pregnancy metabolism. - Source: PubMed
Publication date: 2026/02/03
Li QiuyaZhai PengyanCong DonghangZhang MingZhou Wenbo - Gestational diabetes mellitus (GDM) has a high heritability and frequently co-occurs with type 2 diabetes (T2D), indicating shared genetic mechanisms. Firstly, we employed RHOGE to ascertain the genetic correlation and putative causal directions between GDM and T2D. Subsequently, the Genotype-Tissue Expression Project v8 eQTls files and the FinnGen R11 dataset were employed to conduct cross-tissue transcriptome association studies, Functional Summary-based Imputation in single tissues, and Gene Analysis combined with Multimarker Analysis of Genomic Annotation for GDM and T2D, respectively. A total of 5 genes were identified as GDM susceptibility and 97 genes linked to T2D susceptibility. Of these, four genes (COBLL1, NRBP1, IFT172 and TRIM54) were identified as being shared. Mendelian randomization and colocalization analyses revealed the causal associations of them with GDM and T2D in distinct tissues. Subsequent analyses indicated COBLL1 may influence GDM and T2D risk by regulation of actin filament polymerization and interactions with chemical responses. NRBP1 may confer protective effects against diabetes through regulation of insulin secretion, while IFT172 and TRIM54 may play a role in energy balance signaling and metabolism of skeletal muscle, respectively. Our study provides insight into the shared genetic mechanism between GDM and T2D and identifies potential targets for pharmacological intervention. - Source: PubMed
Publication date: 2026/01/15
Fu LiwanHan XiaodiWang YuquanHu Yue-Qing - The early detection and precise treatment of gastric cancer (GC) remain critical challenges worldwide. In this work, we screened and identified a subset of highly aggressive GC cell lines that exhibit elevated expression of TRIM24 using transwell assays and animal models. TRIM24 showed enhanced expression in GC cells and gastric carcinoma tissue samples in comparison with gastric noncancerous tissues. Importantly, elevated TRIM24 levels correlated with advanced tumor stage and poorer clinical outcomes. Functionally, TRIM24 acted as an oncogene, driving GC proliferation, invasion, and metastasis both in cell culture and animal experiments. Notably, TRIM24 knockdown markedly inducted apoptosis in GC cells through the modulation of NRBP1, a known context-specific tumor suppressor. Mechanistically, TRIM24 bound to NRBP1, enhancing its ubiquitination and subsequent degradation. Further mechanistic insights revealed that NRBP1 phosphorylation at residue S42 was crucial for TRIM24-mediated ubiquitination, with residue K430 identified as the specific ubiquitination site targeted by TRIM24. Jointly, the above findings unveil a critical role for TRIM24 in GC tumorigenesis and metastatic progression, thereby positioning TRIM24 as a promising therapeutic target in GC management. - Source: PubMed
Publication date: 2025/12/22
Weng ChunyanXu JingliHe ChenghaiJin RijuanJin XiaoliangSun ShaopengPan SiweiLi MengHu YueWang XiZhang YanqiangHu CanXu ZhiyuanLv Bin