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
- Per- and polyfluoroalkyl substances (PFAS) are omnipresent, persistent contaminants associated with rising ovarian cancer incidence; however, the molecular circuitry linking PFAS to ovarian tumorigenesis remains obscure. - Source: PubMed
Publication date: 2026/08/28
Wang YuluLiu XueliDing YananZhao ZhanjieChen HaotianWu XiaojuanYang YanzhouPan PenggeLi LuyiGao Hui - Atherosclerosis (AS) is the core pathological foundation of cardiovascular and cerebrovascular diseases, and its efficient prevention is pivotal to lowering related mortality and disability. confers remarkable cardiovascular protection, whereas its anti-atherosclerotic efficacy and intrinsic mechanisms remain poorly elucidated, restricting its clinical translation. This study sought to decipher the mechanism underlying mediated AS improvement via multidimensional artificial intelligence (AI) computation integrated with experimental validation. - Source: PubMed
Publication date: 2026/07/06
Gu LeiLi HengHu YiFan JundeYan LeiXiong QingpingLi LiweiLi YifeiBo LinSui Xuemei - Osteoclasts are responsible for bone resorption, and their excessive activation causes bone loss and structural damage in osteoporosis. Palmitoylethanolamide (PEA), an endogenous PPAR-α agonist, exerts anti-inflammatory effects, but its role in osteoporosis remains incompletely understood. - Source: PubMed
Publication date: 2026/09/07
Xiong FeiYang Liuqing - 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