IRF6 antibody - middle region (ARP31995_P050)
- Known as:
- IRF6 (anti-) - middle region (ARP31995_P050)
- Catalog number:
- arp31995_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- IRF6 antibody - middle region (ARP31995_P050)
Related genes to: IRF6 antibody - middle region (ARP31995_P050)
- Gene:
- IRF6 NIH gene
- Name:
- interferon regulatory factor 6
- Previous symbol:
- VWS, LPS
- Synonyms:
- OFC6, VWS1
- Chromosome:
- 1q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-16
- Date modifiied:
- 2016-10-05
Related products to: IRF6 antibody - middle region (ARP31995_P050)
Related articles to: IRF6 antibody - middle region (ARP31995_P050)
- Human unilateral cleft lip morphopathogenesis is a complex process involving multiple genes and proteins. Factors such as myosin heavy chain 3 (), interferon regulatory factor 6 (), and Gremlin 1 () are implicated in craniofacial development; however, their precise role in unilateral cleft formation remains unclear, limiting improvements in treatment strategies. Immunohistochemistry (IHC) for MYH3, IRF6, and GREM1 proteins and chromogenic in situ hybridization (CISH) for and genes were used to analyze postnatal unilateral right cleft lip tissue (ten patients) and control tissue (six patients). The semi-quantitative counting method was applied, followed by statistical analysis. IHC revealed increased MYH3 expression in cleft muscle tissue and elevated IRF6 expression in the epithelium, whereas GREM1 showed low expression, with significant differences in connective tissue. demonstrated increased gene expression in the cleft epithelium, whereas expression did not differ from controls. Multiple statistically significant correlations were identified, highlighting their potential involvement in cleft morphopathogenesis. - Source: PubMed
Publication date: 2026/05/07
Rone Alise ElizabeteJunga AnnaAkota IlzePilmane Mara - Children with intellectual disability are more likely to experience chronic and neuropathic pain, which remains frequently under-recognized due to limitations in self-reporting and objective assessment tools. Epigenetic mechanisms, particularly DNA methylation, are believed to influence pain perception. This study investigates the differences in methylation patterns between children with intellectual disability and their age- and sex-matched neurotypical controls. - Source: PubMed
Publication date: 2026/05/18
Celsi FulvioZupin LuisaSenn Francescad'Adamo PioCappellani StefaniaDe Zen LuciaCozzi GiorgioSelicorni AngeloBarbi EgidioPeri Francesca - To investigate the mechanisms of histone deacetylase (HDAC) 10 inhibitors (HDAC10Is) action in endometriosis and the target molecules of HDAC10Is. - Source: PubMed
Aso SakiKurogi ShusakuKubo ShuichiHijiya NaokiAoyagi YokoKai KentaroKobayashi EijiNasu Kaei - Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease globally, yet effective therapeutic options remain limited. Red-fleshed apples are rich in dietary flavonoids, but their chemical basis and therapeutic potential for MASLD have not been systematically explored. This study integrated LC-MS/MS metabolomics with a high-fat diet (HFD)-induced MASLD mouse model to evaluate the therapeutic effects and mechanisms of 'XJ4' red-fleshed apple flavonoid extracts (RAFEs). Metabolomics identified 120 types of flavonoids in white-fleshed apple 'FJ' and red-fleshed apple 'XJ4', and 57 differentially accumulated metabolites have been detected in both, among which 39 flavonoids significantly accumulated higher in 'XJ4'. Compared with 'FJ', 'XJ4' was predominantly enriched in -glycosylated flavonols, including isorhamnetin 3--glucoside, cacticin, tamarixin, reynoutrin, and guaijaverin. Male ICR mice were randomly divided into nine groups ( = 10): three groups, normal control, HFD model control, and positive control, receiving simvastatin, 10 mg kg, and six groups receiving RAFEs or white-fleshed apple flavonoid extracts (WAFEs) at low, medium, or high doses (1, 3 and 5 mg kg). Hepatic parameters were assessed by histopathological analysis, biochemical assays, RT-qPCR, immunofluorescence, and western blot analysis; the gut microbiota composition was analysed by 16S rRNA gene sequencing. Medium-dose RAFEs (3 mg kg) conferred optimal efficacy, significantly reducing body weight gain, liver coefficient, and plasma ALT, AST, and ALP levels while restoring the hepatic histological architecture. Mechanistically, RAFEs suppressed pro-inflammatory mediators (IL-6, IL-1β, NF-κB, IRF6 and TLR4) and the oxidative stress marker CYP2E1, while enhancing antioxidant capacity (SOD, CAT and T-AOC). RAFEs also reduced hepatic TG, TC, and LDL-C, increased HDL-C, and modulated lipid metabolism AMPK and PPAR-α upregulation with α-SMA suppression. Furthermore, RAFEs restored gut microbiota diversity, enriched beneficial taxa (, and ), and suppressed pathogenic . RAFEs consistently outperformed WAFEs, attributable to XJ4's unique isorhamnetin-dominated flavonol glycoside profile. These findings support red-fleshed apple flavonoids as promising natural agents for MASLD treatment. - Source: PubMed
Publication date: 2026/05/12
Chen YizhouDong YaqiFan ZhaozhengJiang ShenghuiWu YaWang ChengkunZhu TongyaoWang ZhongkangGuo ShaoxiaZhang YugangLiang Xiao - Erythroid acute myeloid leukemia (AML) cell line OCI-M2 expresses a particular oncogenic network: IRF6, in concert with ETV2 and HEY1, aberrantly activates NKL homeobox gene NKX2-4, which in turn represses megakaryocytic lineage factor FLI1. Interestingly, in keratinocytes, IRF6 is able to bind glucose which promotes IRF6-dimerization and thus alters its binding site selection. Here, we used OCI-M2 as a model to investigate the role of glucose level and IRF6 in leukemogenesis. Treatment of OCI-M2 with high glucose or 2-deoxy-glucose resulted in the downregulation of IRF6 and NKX2-4, and the upregulation of FLI1, indicating that glucose-mediated dimerization of IRF6 altered its reported autoactivation. The screening of this cell line for genes encoding glycolytic enzymes identified aberrant overexpression of glucose-6-phosphate isomerase (GPI) and phosphofructokinase L (PFKL), which were targeted by genomic amplification and chromothripsis-like alterations, respectively. Furthermore, GPI was activated by NKX2-4 and ETV2, and PFKL by ETV2. Finally, siRNA-mediated downregulation of PFKL resulted in elevated glucose levels, suppressed expression of IRF6 and NKX2-4, and activated FLI1. Thus, we connected an oncogenic regulatory network with deregulated glycolytic enzymes and glucose metabolism, thereby establishing a new in vitro model to develop novel therapeutic avenues in AML subsets. - Source: PubMed
Publication date: 2026/03/23
Nagel StefanMeyer CorinnaPommerenke Claudia