RXRB antibody - N-terminal region (P100796_P050)
- Known as:
- RXRB (anti-) - N-terminal region (P100796_P050)
- Catalog number:
- p100796_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RXRB antibody - N-terminal region (P100796_P050)
Ask about this productRelated genes to: RXRB antibody - N-terminal region (P100796_P050)
- 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 antibody - N-terminal region (P100796_P050)
Related articles to: RXRB antibody - N-terminal region (P100796_P050)
- Specific gut microbes are critically involved in the development of metabolic diseases, particularly obesity. Here, through analyses of diabetic patients and animal models, we identified Romboutsia ilealis as a novel gut bacterium that alleviates obesity and associated metabolic disorders by suppressing intestinal lipid absorption rather than altering energy expenditure. Metabolomic profiling revealed 2-oxoindole-3-acetate (OAA) as a key mediator of this effect, which was validated both in vitro and in vivo. Mechanistically, biotin-labeled OAA pull-down coupled with proteomics in the intestinal IPEC-J2 cells identified a direct interaction between OAA and the 26S proteasome subunit PSMD3, leading to destabilization of the mA-binding protein YTHDF2. Loss of YTHDF2 derepressed Rxrb mRNA, increasing CD36 and FABP2 expression and thereby promoting intestinal lipid absorption. Together, our findings uncover a previously unrecognized R. ilealis-OAA-PSMD3-YTHDF2-Rxrb signaling axis that links the gut microbiota to host metabolism, and highlight R. ilealis and OAA as potent next-generation probiotic or metabolite-based therapies for obesity. - Source: PubMed
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Zhu LuoyiHuang LiangLiu ShuqiLuo ShiqiLi YigeWang YizhenZong Xin - Cardiac arrhythmias pose a major health concern while the role of antidiabetic medications in cardiac arrhythmic risks is not fully understood. - Source: PubMed
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Song Zheng-QiZhou Zhi-BoWang Bo-XiangWu Sheng-KeSun Yi-HanChen Yi-HeFeng Su-YinSun Run-Feng - Certain types of antidiabetic drugs (ADs) have been proven to improve cognitive functions and symptom dimensions in schizophrenia (SCZ). - Source: PubMed
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Huang Yu-ShengLin XuXu Ya-JuanChen Gui-Bing - Hypersensitivity reactions (HRs) to non-steroidal anti-inflammatory drugs (NSAIDs) constitute a significant clinical concern due to their frequency and possible severity. These reactions may involve specific immunological pathways, including activation of the high-affinity IgE receptor, or non-immunological mechanisms that result in similar clinical manifestations. Additionally, vitamin D plays an important role in the regulation of the immune response and therefore may be relevant to the development or progression of HRs to NSAIDs. - Source: PubMed
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Amo GGarcía-Menaya J MMartí MGómez-Tabales JCornejo-García J ABlanca-López NCanto GDoña IBlanca MTorres M JAgúndez J A GGarcía-Martín EAyuso P - Primary sclerosing cholangitis (PSC) is a kind of cholestatic liver disease without effective targeted therapies, and its pathogenesis remains largely unclear. We performed genome-wide Mendelian randomization analysis to identify therapeutic targets PSC risk. Summary statistics for PSC were obtained from 2 datasets: the International PSC Study Group (2871 cases and 12,019 controls) and the FinnGen cohort (1483 cases and 361,641 controls). Cis-expression quantitative trait loci for druggable genes were extracted from the eQTLGen Consortium and Genotype-Tissue Expression Version 8 database and applied as genetic instrumental variables. Colocalization analysis was performed to estimate the probability that single nucleotide polymorphisms associated with PSC and eQTLs shared causal locus. Six drug targets (APOM, BTN3A2, HLA-DRA, membrane metalloendopeptidase like 1 [MMEL1], NEU1, and RXRB) presented significant Mendelian randomization results in 2 independent datasets. MMEL1, of which eQTLs resourced from blood, liver, transverse colon, and intestine, was all found to have strong evidence for colocalization with PSC. Genetically proxied inhibition of MMEL1 was also detected to attenuate the risk of immune bowel diseases and ulcerative colitis. A transcriptome-wide associated study presented consistent inference, as shown above. Our study highlighted 1 candidate druggable target (MMEL1 for PSC development and prognosis). - Source: PubMed
Li Chang-LeiSun AoLiu Yu-KunSun Rui-TaoHao Ao-YunLan Ying-YingCao Jing-YuWang Zu-Sen