Ask about this productRelated genes to: RXRA Blocking Peptide
- Gene:
- RXRA NIH gene
- Name:
- retinoid X receptor alpha
- Previous symbol:
- -
- Synonyms:
- NR2B1
- Chromosome:
- 9q34.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2016-10-05
Related products to: RXRA Blocking Peptide
Related articles to: RXRA Blocking Peptide
- Gaseous air pollution is a major environmental risk factor for atherosclerosis, yet the specific molecular networks linking Gaseous air pollution to atherosclerosis are not fully characterized. This study aimed to elucidate how gaseous pollutants drive atherosclerosis using a multi-level framework integrating network toxicology, nine machine-learning algorithms, bulk and single-cell/spatial transcriptomics, molecular docking, clinical tissue/serum validation, and in vitro pollutant-exposure assays. A conserved -- axis was identified as a core molecular network linking pollutant exposure to atherosclerosis. Single-cell and spatial transcriptomics showed broad expression of () in vascular stromal and endothelial cells and its association with xenobiotic and lipid metabolism, whereas () and () were enriched in macrophages, T cells, and mast cells within plaques, correlating with immune cell infiltration. Multiple pollutants displayed high binding affinity to these proteins. Clinical samples showed upregulation of these targets in atherosclerotic tissue and serum. Toluene exposure in THP-1-derived macrophages significantly increased , , and mRNA and protein levels. These findings highlight an immune-metabolic interplay centered on the -- axis in Gaseous air pollution-driven atherosclerosis, supporting these molecules as candidate biomarkers for environmental health strategies. - Source: PubMed
Publication date: 2026/08/18
Hai HusilengWang QianheLi JuanWang JieJiang XijuanGuo Maojuan - BH3 mimetics are a promising class of drugs in hematologic malignancies, but their efficacy in peripheral T-cell lymphoma (PTCL) remains poorly understood. To identify genetic determinants of BH3 mimetic response, we performed a genome-wide CRISPR-Cas9 knockout screen in PTCL cell lines and identified MYLIP, an E3 ubiquitin ligase targeting the LDL receptor (LDLR), as a novel sensitizer to navitoclax. MYLIP deletion enhanced the cytotoxicity of navitoclax, venetoclax, and the BCL-XL-selective degrader DT2216 across multiple PTCL models. Mechanistically, MYLIP loss increased LDLR expression, promoted cholesterol uptake, and elevated apoptotic priming. Recombinant PCSK9, which facilitates LDLR degradation, reversed MYLIP knockout-induced sensitization, establishing a functional role for LDLR in BH3 mimetic response. We also identified the nuclear receptor RXRB as an upstream regulator of MYLIP; dual RXRA/RXRB depletion more effectively suppressed MYLIP, upregulated LDLR, and potentiated navitoclax cytotoxicity. In vivo, MYLIP-deficient xenografts showed enhanced tumor suppression with navitoclax treatment. Transcriptomic analyses of primary PTCL samples revealed reduced MYLIP expression in ALK-positive anaplastic large cell lymphoma and genetically defined subsets of nodal T follicular helper cell lymphomas. These findings uncover an RXR-MYLIP-LDLR axis that links cholesterol metabolism to apoptotic susceptibility, offering mechanistic insight into BH3 mimetic sensitivity in PTCL. - Source: PubMed
Publication date: 2026/08/25
Yokoyama KeitoChiba MasahiroTakei NorioSuto KeitoIshio TakashiGoto HidekiEndo TomoyukiKadin Marshall EMaeda MichiyukiWatanabe MasashiHatakeyama ShigetsuguTeshima TakanoriYang YibinNakagawa Masao - Perfluoroalkyl and polyfluoroalkyl substances (PFAS), man-made fluorinated chemicals, are widely distributed in the environment and can enter human habitats through various pathways. However, the mechanisms by which PFAS affect metabolic health are not fully understood. - Source: PubMed
Publication date: 2026/08/25
Qiao ZipengLiu TaoHu XiongfeiNi WeiweiJiang BohanLu Chan - Diabetic osteoporosis (DO) is a chronic consequence of diabetes mellitus marked by disrupted bone metabolism and elevated fracture risk, with no effective strategies currently available. Betulinic acid (BA) is a natural pentacyclic triterpenoid demonstrating anti-diabetic, anti-inflammatory, and osteoprotective effects. This research aimed to clarify the molecular mechanisms of BA in DO using network pharmacology, molecular docking, and molecular dynamics simulations. - Source: PubMed
Publication date: 2026/08/06
Sharma SheenamChaudhary RishabhSharma ChiragDabral SwarnaBansal SeemaSharma NeelamGupta Sumeet - Gouteng is a traditional Chinese medicine widely used for the clinical treatment of epilepsy, yet the specific mechanism underlying its antiepileptic has not been elucidated. Network pharmacology, bioinformatics, machine learning, molecular docking, MD simulation, and ADMET druggability analysis were performed to systematically elucidate the molecular regulatory mechanism of Gouteng against epilepsy. The results showed that 29 active components of Gouteng collectively regulated 661 potential antiepileptic targets. Through screening with machine learning-based disease diagnostic model, MDM2 and PPARG as the core target genes mediating the antiepileptic effect of Gouteng were finally identified. Immune infiltration analysis confirmed that MDM2 and PPARG synergistically reshape the immune microenvironment of epileptic lesions, restrain excessive inflammatory responses, and maintain immune homeostasis and tolerance. Molecular docking and MD simulation revealed that the four core active components, namely Angustidine, Rhynchophylline A, vincoside lactam_qt, and coryincine, target the hydrophobic pocket of MDM2, with non-polar interactions serving as the primary driving factor for their interactions. ADMET analysis indicated that vincoside lactam_qt and coryincine exhibit favorable oral bioavailability, excellent blood-brain barrier permeability, and low hepatotoxicity, which make them potential antiepileptic candidate drugs with clinical translational potential. Most importantly, Gouteng exerts antiepileptic effects by targeting and regulating the dual MDM2-MDM4/TP53 and PPARG-NCOA1/RXRA regulatory axes, thereby mediating neuroinflammation inhibition and neuronal protection. Furthermore, TFAP2C as a common upstream transcription factor of both MDM2 and PPARG was identified. This study provides theoretical basis for the development of novel MDM2/PPARG-targeted antiepileptic drugs and for the clinical application of Gouteng. - Source: PubMed
Publication date: 2026/08/10
Zhang Hong-QuanChen LinYuan Xian-JunLuo Yao-XueDuan Li-XinLin Ya-QiWang Rui-Ge