Human forkhead box O3,FOXO3 ELISA Kit
- Known as:
- Human forkhead box O3,FOXO3 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-0627
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human forkhead box O3 FOXO3 ELISA Kit
Related genes to: Human forkhead box O3,FOXO3 ELISA Kit
- Gene:
- FOXO3 NIH gene
- Name:
- forkhead box O3
- Previous symbol:
- FKHRL1, FOXO3A
- Synonyms:
- AF6q21, FOXO2
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-23
- Date modifiied:
- 2015-08-25
Related products to: Human forkhead box O3,FOXO3 ELISA Kit
Related articles to: Human forkhead box O3,FOXO3 ELISA Kit
- The imbalance of pro-inflammatory and immunosuppressive constituents in the tumor microenvironment (TME) significantly dictates cancer progression, immune invasion, and treatment response. Immunosuppressive regulatory T cells (Tregs) are associated with decreased disease-free survival due to their ability to suppress anti-tumor immunity. Notably, in response to environmental cues, Tregs display functional and phenotypic plasticity with inflammatory helper T cell subsets. Given their predominant role in sustaining immune suppression, it is remarkable that multiple developmental pathways converge to regulate Treg development and function. In this study, we designed, validated, and employed a novel genetically modified mouse model to conditionally ablate the Hedgehog (Hh) gene, Gli2, specifically in Tregs. Ablation of Gli2 activity in Tregs significantly reduced tumor burden, impaired Treg suppressive function, and shifted the transcriptional balance of Foxo3 and Rorγt, transcription factors essential for Tregs and Th17 cells. Spatial mapping highlighted that Gli2 ablation in Tregs enhances the immunogenicity of the tumor and promotes a pro-inflammatory milieu of the TME. This was underscored by a higher tumor immune signature score and enhanced infiltration of cytotoxic CD8 T cells into the tumor. These findings highlight Hh/Gli2 signaling in Tregs as a mechanistic regulator of immunogenicity in the TME and a potential therapeutic target to prime tumors for enhanced responsiveness for adjuvant treatments. - Source: PubMed
Publication date: 2026/07/06
Swain Courtney AHinshaw Dominique CMiranda Ian DMetge Brandon JElhamamsy AmrChen DongquanLee AlyssaGuo HuaPapineni BhavyasreeWilliams Li'anRathmell Jeffrey CPonnazhagan SelvaranganWelner Robert SSamant Rajeev SShevde Lalita A - Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a severe extra-articular manifestation with limited treatment options. Identifying anti-arthritic agents that concurrently protect against ILD is clinically significant. Sinomenine (SIN), a natural alkaloid used clinically to treat RA, shows potential anti-fibrotic activity, but its efficacy and mechanism in RA-ILD remain unclear. Here, integrative bioinformatic analyses identified ILD-associated signature characterized by upregulated CHRNA7 (encoding α7nAChR) and downregulated GLUL, specifically in pulmonary fibroblasts and myofibroblasts, and GLUL was a crucial mediator between RA and ILD. In the adjuvant-induced arthritis (AIA) model with pulmonary inflammatory and fibrotic remodeling, the phenotype that recapitulates early-stage RA-ILD, pulmonary ACh and α7nAChR expression were observed upregulated. SIN ameliorated arthritis and pulmonary lesions, suppressed pulmonary α7nAChR signaling, inhibited AKT/FOXO3 activation, restored GLUL expression and improved autophagy-related changes in this model. Microscale thermophoresis (MST), molecular docking and molecular dynamics simulation supported a direct binding between SIN and α7nAChR. In vitro, α7nAChR activation with PNU-282987 promoted fibroblast-to-myofibroblast transition (FMT), whereas its genetic knockdown inhibited FMT, suppressed AKT/FOXO3 activation, and restored GLUL expression in TGF-β-stimulated MRC-5 cells. We confirmed direct FOXO3 binding to the GLUL promoter by ChIP-qPCR. SIN inhibited FMT and regulated the AKT/FOXO3/GLUL axis in an α7nAChR-dependent manner. Pharmacological inhibition and siRNA-mediated knockdown of GLUL abolished SIN-mediated regulation of mTOR-autophagy signaling and FMT. Our findings identify the α7nAChR/AKT/FOXO3/GLUL axis as a novel fibrotic driver and highlight SIN as a potential therapeutic candidate to inhibit RA-ILD by targeting this axis. - Source: PubMed
Publication date: 2026/07/04
Liu MuqiuDu HuaizhiZheng JunhuiLiu MinJiang ZhihaoHuang JieyingJiang SiheYi LangZhang LingyuLi YanwuDu QunLiu LiangNi HaojieZhang XiaojunZhou HuaDong Yan - Sepsis-induced cardiomyopathy (SICM) is a life-threatening complication of sepsis characterized by acute and reversible myocardial dysfunction, for which effective targeted therapies remain limited. Artesunate (ART), a well-established first-line antimalarial agent, has attracted increasing attention for its anti-inflammatory, antioxidant, and cytoprotective properties. However, its role in SICM has not been fully elucidated. In this study, a murine SICM model is established using lipopolysaccharide (LPS) to evaluate the effects of ART on animal mortality, cardiac function, histopathology, and biomarkers of myocardial injury. In parallel, the study is performed using neonatal rat cardiomyocytes and H9c2 cells exposed to LPS in the presence or absence of ART. Transcriptomic and metabolomic analyses are used to elucidate the molecular mechanisms underlying ART-mediated cardioprotection. ART administration significantly improves cardiac function, attenuates myocardial injury, alleviates the inflammatory response, and reduces cardiomyocyte apoptosis in LPS-challenged mice. Consistent results are observed . Integrated multi-omics analyses identify the Akt/FoxO3 signaling pathway as a critical target of ART. ART treatment contributes to increased Akt phosphorylation and subsequent suppression of FoxO3 nuclear translocation and its transcriptional activity. Pharmacological inhibition of Akt using MK2206 or genetic knockdown of by siRNA abolishes the cardioprotective effects of ART. In addition, molecular docking analysis suggests a potential interaction between ART and Akt isoforms. Collectively, these findings demonstrate that ART possesses significant cardioprotective effects in experimental SICM through modulation of the Akt/FoxO3 signaling axis, leading to reduced apoptosis and inflammation. ART may serve as a therapeutic candidate for the management of SICM. - Source: PubMed
Publication date: 2026/07/01
Jiang XiChen YankunZeng YalinChen YanghaoYang DanLing Zhiyu - Polycystic ovarian syndrome (PCOS) is a common endocrine-metabolic condition characterized by persistent anovulation, and hormonal imbalance leading to disrupted follicular maturation, and overall ovarian dysfunction. This study aimed to investigate the regenerative effects of adipose-derived mesenchymal stem cell-derived exosomes (AD-MSCs-Exo) on ovarian restoration, and granulosa cells (GCs) functionality in a PCOS murine model. PCOS was induced via a single subcutaneous injection of estradiol valerate. Exosomes were isolated from AD-MSCs using the ExoCIB kit and characterized by DLS, TEM and flowcytometery. NMRI mice received intraperitoneal injection of AD-MSCs-Exo (25, 50, 75, and 100 µg/kg body weight) twice over a two-week period. Following treatment, the mice were anaesthesia and sacrificed by cervical dislocation. The harvested ovarian tissues were subjected to histological assessment; FSH, LH, and estradiol levels were measured from serum. Further, GCs were isolated, and identified through FSH expression. Subsequently, the levels of GCs key regulator genes including FOXO3, Map1lc3b, and SF-1 were assessed by qRT-PCR. AD-MSCs-Exosome-like nanovesicles isolated in range of 30-80 nm with bi-membrane spherical shape and 54.8% expression of CD9. The hormonal analysis revealed improved estradiol levels and a lowered LH/FSH ratio, indicating endocrine stabilization under exposure with AD-MSCs-Exo. In addition, treatment with AD-MSCs-Exo significantly improved ovarian histoarchitecture, and the optimum response was observed following exposure to 75 µg/kg of AD-MSCs-Exo. However, administration of the highest dose (100 µg/kg) was associated with inflammatory responses and partial tissue degeneration. Gene expression analysis also showed a marked up-regulation of FOXO3, along with increased Map1lc3b and SF-1 levels. Accordingly, AD-MSCs-Exosome like nanovesicles at optimum concentration exert regenerative effects on PCOS-induced ovarian dysfunction, which emphasizes the necessity for precise dose selection to achieve maximal therapeutic efficacy as a promising cell-free strategy for PCOS treatment. - Source: PubMed
Publication date: 2026/07/01
Khorram FatemehAmini ElahehAzarnia MahnazNiknejad Azadeh - Olfactory dysfunction is a debilitating condition with no established treatment. This study evaluated the efficacy of intranasal (i.n.) NAD administration in restoring olfactory function. Cultured human olfactory stem cells (hOSCs) were treated with NAD and assessed by immunofluorescence staining, PCR, and western blot analyses. In vivo, mice with ZnSO-induced anosmia were treated with i.n. NAD, intraperitoneal dexamethasone, or PBS and evaluated by histological analysis, behavioral tests, bulk RNA-sequencing (RNA-seq), and in situ hybridization. NAD promoted hOSC differentiation into olfactory sensory neurons (OSNs), evidenced by increased stem cell (SOX2 and nestin) and OSN markers (Tuj1 and OMP) expression, and upregulated neuronal differentiation-related genes (SOX2, NESTIN, NEUROD1, NEUROG1, and OMP). In vivo, the NAD group showed significant olfactory function improvement and marked olfactory epithelium repair. Bulk RNA-seq of the olfactory turbinate tissue identified 113 differentially expressed genes (cluster T1) upregulated in control and NAD groups. The Gene Ontology (GO) term "modulation of chemical synaptic transmission" was associated with cluster T1, and 25 genes implicated in this GO were upregulated in the NAD group. Integration with publicly available single-cell RNA-seq data identified six neuronal marker genes - ABHD2, DLGAP2, FOXO3, HIPK2, KCNMA1, and PCDH17 - upregulated by NAD. Protein expression of DLGAP2 and PCDH17 was higher in differentiated hOSCs treated with NAD. In situ hybridization confirmed that Dlgap2, Foxo3, and Pcdh17 expression was restored in anosmic mice treated with i.n. NAD. The potential therapeutic efficacy of i.n. NAD administration was demonstrated by showing regeneration of OSNs in hOSCs and restoring olfactory function in an anosmia mouse model. - Source: PubMed
Publication date: 2026/07/01
Yoo Shin HyukJang Jung YeonBae Jun-SangVentura ReizaKim Eun HeeKim A YoungMo Ji-HunPark JaewooKang KyuhoYun YeogyunLee Jun HeeKim Yong-JaeLee Dong-JoonKim Ji Heui