Ask about this productRelated genes to: RXRB Blocking Peptide
- Gene:
- RXRB NIH gene
- Name:
- retinoid X receptor beta
- Previous symbol:
- -
- Synonyms:
- NR2B2, H-2RIIBP, RCoR-1
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2016-10-05
Related products to: RXRB Blocking Peptide
Related articles to: RXRB Blocking Peptide
- Aflatoxin B1 (AFB1) is a highly toxic mycotoxin that causes severe renal injury, yet the molecular basis of its nephrotoxicity remains poorly defined. Here, we integrated multi-omics data with computational modeling to elucidate the mechanisms of AFB1-induced kidney damage. Three human renal transplant biopsy microarray datasets (GSE1563, GSE30718, and GSE61739), comprising 121 injury samples and 84 control samples and representing distinct forms of transplant-associated renal injury, including acute rejection and ischemic kidney injury, were analyzed using differential expression and weighted gene co-expression network analyses, which identified 174 injury-related genes. A total of 145 AFB1-associated targets were obtained from multiple public datasets. Intersection analysis between these two gene sets identified RXRB and F11 as core hub genes potentially involved in AFB1-induced renal injury. Immune infiltration and gene set enrichment analyses suggested their involvement in immune regulation and toxicity-related signaling pathways. Molecular docking demonstrated favorable binding of AFB1 to RXRB and F11, with binding energies of -9.9 and -7.4 kcal/mol, respectively, while molecular dynamics simulations further confirmed the stability of these complexes. Together, this integrative multi-omics and modeling approach reveals key molecular determinants of AFB1-induced renal toxicity and offers a theoretical foundation for developing targeted interventions against AFB1-related kidney disorders. - Source: PubMed
Publication date: 2026/08/07
Chen YihuangZhang YuanqunLiu GuohaoLiu Huan - Fat deposition determines beef marbling grade and meat quality, but the underlying molecular mechanisms remain unclear. This study aimed to investigate the role of bovine PPARD in lipid deposition, especially its effect on the expression of fatty acid transport genes (, , and ) and the lipid droplet-associated gene () in liver tissues from cattle with different marbling grades. The mRNA abundance and protein levels in liver tissues from thirty-one Wagyu × Angus crossbred beef cattle (25-26 months old) with different marbling grades (according to GB/T 29392-2022, based on the marbling richness of the longissimus dorsi muscle at the 12th-13th rib interface) were analyzed by RT-qPCR and Western blot, respectively. Additionally, was knocked down and overexpressed in bovine mammary epithelial cells to validate its effects on lipid-metabolism-related genes. The results showed that the mRNA levels of , , , , , and were significantly higher ( < 0.01) in livers tissues from the A3 and A4 groups (high marbling) than in those from the A1 and A2 groups (low to moderate marbling). Western blot analysis revealed significantly higher PPARD protein expression in the A3 and A4 groups (high marbling) than that in the A1 and A2 groups (low to moderate marbling) ( < 0.05). It should be noted that the sample size of Group A4 is only 2, and the results of this group should be considered as a preliminary trend that needs to be validated with larger sample sizes. Cellular experiments confirmed that knockdown significantly decreased mRNA expressions of , , and ( < 0.01), while overexpression significantly increased their mRNA levels ( < 0.05). These results indicate a positive correlation between PPARD expression and the transcriptional levels of genes involved in fatty acid transport and lipid droplet storage, suggesting that PPARD may be associated with hepatic lipid metabolism and potentially contribute to marbling development. These findings suggest that the PPARD signaling pathway contributes to hepatic lipid deposition and may play a role in marbling formation in beef cattle. - Source: PubMed
Publication date: 2026/07/06
Wang KaiyouWang QiWang QinyuTian ShuaiyingQi YingZhang LinXing BaokuiTuliguer Li Qiuling - Frailty is a multidimensional geriatric syndrome that lacks a consistent definition, complicating its clinical management. Epigenetic data suggest that frailty involves altered CpG sites, potentially driven by environmental epigenetic factors (the exposome) that influence aging. Systematically reviewing studies from 2009 to 2025, we quantified frailty prevalence, pooled weighted methylation beta values for associated CpG sites, performed enrichment analysis, and conducted structural network analysis to evaluate chemical interactions, following the PRISMA 2020 guidelines and with the study prospectively registered in PROSPERO (ID 1159037). Results showed a pooled frailty prevalence of 17.4% with extreme heterogeneity (I = 98.88%), and a combined methylated beta effect of -0.1378 (CI: -0.4156, 0.1400) with high heterogeneity (I = 100%), highlighting sources of variability. Interestingly, we found a CpG site (cg04772644) shared between Chinese and German cohorts, and, upon mapping, four frailty-related genes (CDC42BPB, SLC1A5, RXRB, and SLC22A18AS) were shared across cohorts. Indeed, these genes are significantly enriched in pathways including thrombin signaling, G protein-coupled receptor signaling, and immune cell differentiation signaling. Finally, our system toxicology analysis demonstrated that arsenite, bisphenol A, benzamide, dorsomorphin, and trichostatin A directly interact with the four shared genes, suggesting that the chemical exposome contributes to the observed epigenetic heterogeneity of frailty and the concomitant clinical manifestations. - Source: PubMed
Publication date: 2026/07/03
Cedillo-Rivero Alejandro EliuRodriguez-Cuartas Julian DanielGomez-Zapata ValentinaFlores-Soto EdgarGomez-Verjan Juan CarlosRivero-Segura Nadia Alejandra - Chronic non-bacterial osteomyelitis (CNO) is a rare autoinflammatory bone disease primarily affecting children and adolescents. Reliable biomarkers for diagnosis, disease monitoring, and prediction of disease course are lacking. This study demonstrates that, when compared to healthy participants, the proportion of 'pro-inflammatory' CD14CD16 'classical' monocytes is elevated in patients with CNO, before and after the initiation of treatment. Differential DNA methylation (200 hyper-, 162 hypo-methylated) profiles in monocytes from CNO patients affect key genes involved in immune regulation, including RUNX3, HOXA9, HLA-DMB, HLAB, MAP3K6, RXRB, CD163L1, MAP2, CDK6, HLA-G, HDAC10, and HLA-DQA1 genes. Notably, DNA methylation changes persist and potentially progress over time after the initiation of treatment with naproxen. In conclusion, patients with CNO display higher proportions of 'classical' monocytes when compared to healthy participants in conjunction with dysregulated DNA methylation patterns. Molecular alterations remain despite symptom relief with naproxen, suggesting progressive inflammation-mediated changes. - Source: PubMed
Publication date: 2026/05/15
Carlsson EmilGodoy-Tena GerardMorbach HennerGirschick Hermann JDissanayake DilanCharras AmandineBallestar EstebanHedrich Christian M - Chronic myeloid leukemia (CML) is a hematological malignancy that has its cause as Philadelphia chromosome and BCR: ABL fusion gene. Although specific drugs such as imatinib have been used to a great effect to enhance the outcome of treatment, resistance is still a challenge especially in later stages of the disease. This work has explored the phenotypic role of eight single nucleotide variants (SNVs) in the downstream sequence of MIR5195 gene, which are determined in real-life sample of patients. The initial experiment involved whole-exome sequencing (WES) to identify genetic variants in advanced phase CML patients and Sanger sequencing to validate the variants. The results indicate the possible importance of the established mutations as well as mutations that are yet to be characterized in the regulation of MIR5195 and their potential impact on the development of CML. Comprehensive bioinformatics analyses (MEME, TOMTOM, and RegulomeDB) revealed that these mutations profoundly reconfigure local cis-regulatory architecture, resulting in the loss of conserved transcription factor binding motifs and the emergence of a mutation-specific motif enriched for hematopoietic and cancer-associated transcription factors, including RXRB, FOXP1, GATA-1, and GATA-2. Three-dimensional structural modeling using AlphaFold3 showed that both wild-type and mutant downstream MIR5195 sequences retain canonical B-form DNA, but the mutant exhibits localized changes in backbone curvature and groove geometry within the mutation-enriched motif. Molecular docking analyses revealed transcription factor–specific redistribution of binding affinities rather than uniform loss of interaction, with increased binding observed for GATA1 (− 242.20 vs. − 228.26) and RXRB (− 223.57 vs. − 221.44), and reduced binding for FOXP1 (− 213.63 vs. − 219.93) and GATA2 (− 242.15 vs. − 281.57). These findings indicate selective modulation of transcription factor engagement driven by downstream non-coding mutations. Based on the emergence of a mutation-specific regulatory motif, we designed a transcription factor decoy oligonucleotide targeting the altered binding site as a potential mutation-directed regulatory strategy. Overall, this integrative computational and experimental framework demonstrates that downstream MIR5195 mutations quantitatively reprogram transcription factor binding networks in CML and highlights non-coding regulatory variation as a biologically meaningful contributor to leukemia pathogenesis. - Source: PubMed
Publication date: 2026/04/11
Shahid SameenSabar Muhammad FarooqIqbal Zafar