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
- Acetaminophen (APAP) overdose can induce hepatic injury and even acute liver failure. Astragaloside IV (AS-IV), a saponin isolated from Astragalus membranaceus, demonstrates protective effects on both digestive and immune systems owing to its antioxidant and anti-inflammatory properties. This study aims to investigate the protective effects and underlying mechanisms of AS-IV against APAP-induced liver injury (AILI) in mice. Potential therapeutic targets of AS-IV against AILI were predicted through network pharmacology and GEO data mining. Functional enrichment analysis was performed on the identified targets. Molecular docking and dynamics simulations were conducted to validate the binding interactions between AS-IV and core targets within the PPAR signaling pathway. For in vivo validation, fifty C57BL/6 mice were randomly allocated into five groups: control, APAP model, AS-IV low-dose, AS-IV high-dose, and N-acetylcysteine treatment groups. Following model establishment, serum AST and ALT levels were measured to assess liver function. Hepatic histopathological changes were evaluated by HE staining, while RT-qPCR and WB were employed to quantify the expression of key genes and proteins. Network pharmacology analysis identified 43 potential therapeutic targets of AS-IV against AILI, including key molecules such as IL1B, PPARG, RXRA, and FOS. KEGG pathway enrichment revealed significant associations with the PPAR signaling pathway, measles, and non-alcoholic fatty liver disease. In vivo experiments demonstrated that AS-IV treatment effectively attenuated histopathological liver damage in AILI mice, as evidenced by significantly reduced serum ALT and AST levels. Furthermore, AS-IV administration markedly upregulated both mRNA and protein expression levels of critical metabolic regulators PCK1, RXRA, and PPARG. In conclusion, AS-IV alleviates AILI by modulating the PPAR signaling pathway through regulation of PCK1, PPARG, and RXRA. - Source: PubMed
Jiang ShunleiRen XiaGao XinZhou YuhongZhou JiachengChen ChengQiu YuezhiHan LiangZhao ZhiqiangLi Jixu - We investigated the conformational mechanisms underlying PPARγ activation in muscle-invasive urothelial carcinoma (MIUC) and sought to develop covalent inverse agonists to therapeutically reinforce a repressive state. The integration of mutational, structural, and biochemical analyses of PPARγ and RXRα guided the discovery of FX-909, a first-in-class clinical PPARγ inverse agonist that enforces a repressive conformational state, even in highly activated biological contexts. FX-909 is a potent, highly selective, and powerful suppressor of PPARγ transcriptional activity through the enhancement of PPARγ-nuclear co-repressor (NCOR) binding affinity. Treatment with FX-909 resulted in selective growth inhibition in PPARγ-activated MIUC cell lines and durable regressions in xenograft models of MIUC. FX-909 is capable of recapitulating PPARG genetic knockout phenotypes in vivo and is currently in clinical development for the treatment of intractable MIUC. - Source: PubMed
Publication date: 2026/05/28
Stuckey Jacob IMertz Jennifer AWilson Jonathan EWilliamson Kaylyn ELi YongKuljanin MiljanSetser Jeremy WDeLaBarre ByronChenail GreggNguyen Phuong AScott Mark EGeier Michael JBailey Christopher MMotley William WAudia James ESims Robert J - Acquired resistance to cisplatin-based chemotherapy is common in patients with gastric cancer (GC) and significantly limits treatment efficacy. The aim of this study was to investigate molecular features associated with GC chemoresistance using an integrative multi-level analytical framework combined with Mendelian randomization (MR), followed by cellular validation of key candidates. - Source: PubMed
Publication date: 2026/05/01
Tao ShuchangYang Hui - Central to the pathogenesis of type 2 diabetes (T2D) is the failure in insulin secretion from pancreatic β-cells associated with insulin resistance. The nuclear receptor RXRA/RXRα (retinoid X receptor alpha) is a transcriptional regulator of insulin secretion and systemic glucose metabolism. Here, we show that the macroautophagic/autophagic receptor SQSTM1/p62 (sequestosome 1) sequesters RXRA for lysosomal degradation to modulate glucose metabolism and insulin secretion. Under glucolipotoxicity, RXRA is released from SQSTM1 to inhibit mitochondrial respiration and insulin secretion and to induce lipogenesis. SQSTM1-dependent degradation of RXRA was reconstituted and mice using ATB1002, a chemical N-degron designed to bind and activate SQSTM1 as an N-recognin of the N-degron pathway. In prediabetic and T2D models, SQSTM1 agonists induced the lysosomal degradation of RXRA, and enhanced glucose-stimulated insulin secretion and insulin responsiveness. These results identify SQSTM1 as a master regulator in glucose metabolism and insulin secretion, providing a therapeutic means to treat T2D.: ATLs: autophagy targeting ligands; AUC: area under the curve; ATP: adenosine triphosphate; co-IP: co-immunoprecipitation; GSIS: glucose-stimulated insulin secretion; GTT: glucose tolerance test; HFD: high-fat diet; i.p.: intraperitoneally; LBD: ligand binding domain; NR1H3/LXRα: nuclear receptor subfamily 1 group H member 3; Nt: N-terminal; PPARG/PPARγ: peroxisome proliferator activated receptor gamma; RER: respiratory exchange ratio; RXRA/RXRα: retinoid X receptor alpha; SQSTM1/p62: sequestosome 1; T2D: type 2 diabetes; TG: triglycerides; TIW: three times per week; UBA: ubiquitin-associated domain; ZZ: zinc finger. - Source: PubMed
Publication date: 2026/05/25
Jung Eui JungKim Hye YeonBae Tae HyunChoi Eun NamLim HyominKim MinjiMun Su RanLee Yoon JeeHahn SoojungLee Dong RyulPark Woo-JaeSuh Young HoKwon Yong TaeSon Yeon SungKim Hee-YeonPark Joo-Won - - Source: PubMed
Publication date: 2026/05/12
Ma LinaWu Min