Mouse forkhead box O4,FOXO4 ELISA Kit
- Known as:
- Mouse forkhead box O4,FOXO4 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0998Mo
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- Sunlog
- Gene target:
- Mouse forkhead box O4 FOXO4 ELISA Kit
Related genes to: Mouse forkhead box O4,FOXO4 ELISA Kit
- Gene:
- FOXO4 NIH gene
- Name:
- forkhead box O4
- Previous symbol:
- MLLT7
- Synonyms:
- AFX1
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-14
- Date modifiied:
- 2014-11-18
Related products to: Mouse forkhead box O4,FOXO4 ELISA Kit
Related articles to: Mouse forkhead box O4,FOXO4 ELISA Kit
- Gene transcription is a stochastic bursting process with burst frequency and size as core parameters. While complex models capture detailed biology, their computational cost limits genome-wide applications. We propose a simple telegraph model-based framework to analyze genome-wide scRNA-seq datasets. When sample size ≥500 and burst parameter change ≥ 3 fold, inferred burst frequency- and size-dominated variations reliably proxy true regulation. Analyses across mouse cells and healthy/hypertrophic cardiomyopathy (HCM) human heart tissues revealed three conserved principles: (1) over 70% of genes with altered burst regulation exhibited burst frequency- or size-dominated regulation; HCM genes show stronger bursting featuring prolonged inactivity and intense transcription; (2) TATA-initiator synergy is lost in HCM; and (3) burst frequency-dominated genes enriched in genome stability/cell cycle/apoptosis (via TFs like /), while burst size-dominated ones enrich in signaling/metabolism (via TFs like /). Their interdependent dysregulation accelerated HCM. This study establishes the simple telegraph model as a scalable framework linking transcriptional burst dynamics to cell fate and pathology. - Source: PubMed
Publication date: 2026/08/11
Chen LiangWu YuwenYang ChengkaiFang SijiaLiao YuWu YuehengZhang HongkunJiang GuozhiYu JiansheJiao Feng - Diabetic nephropathy (DN) represents the leading cause of end-stage renal disease; however, its molecular mechanisms remain incompletely understood. This study aims to elucidate the specific roles and regulatory mechanisms of Tissue factor pathway inhibitor 2 (TFPI2) and forkhead box O4 (FOXO4) in DN. - Source: PubMed
Publication date: 2026/08/20
Mu LiqinZhao YuLi YangGao WeiWang Jing - High-fat diets are increasingly used in aquaculture due to their protein-sparing effects; however, the post-transcriptional regulatory mechanisms of fish muscle in response to high-fat diets (HFD) remain unclear. In this study, juvenile black seabream were fed either a normal-fat diet (NFD) or a HFD to investigate the miRNA-mRNA regulatory network associated with diet-induced muscle lipid deposition. Oil Red O staining and biochemical analysis showed that high-fat diet feeding markedly increased lipid droplet accumulation and crude lipid content in muscle, indicating significant induction of muscle lipid deposition. Integrated mRNA and miRNA expression profiling revealed substantial transcriptomic and post-transcriptional responses to high-fat diet challenge. A total of 271 differentially expressed genes were identified, including 120 upregulated and 151 downregulated genes. Through combined target prediction and expression correlation analysis, thirteen candidate inverse miRNA-mRNA relationships were subsequently identified, and RT-qPCR supported the expression patterns of selected miRNAs and mRNAs. These pairs included miR-499-x-dmgdh, miR-499-y-gatm, miR-727-y-ass1, miR-4649-x-foxo4, miR-9129-z-myl7, and several novel miRNA-mediated interactions involving adk, chst11, lypla2, frem2, kcnc4, wars1, bag2, and capn2. Functional analysis suggested that these regulatory pairs were mainly associated with metabolic adaptation, structural remodeling, and cellular stress responses. In particular, gatm, dmgdh, ass1, and adk were associated with energy metabolism-related processes, including pathways previously linked to Ampk regulation, whereas myl7, frem2, and kcnc4 may contribute to muscle structural maintenance and excitability regulation. Overall, this study provides candidate miRNA-mRNA regulatory relationships potentially involved in high-fat diet-induced muscle lipid deposition and adaptive remodeling in black seabream, offering a basis for future functional studies on muscle metabolism and quality regulation in marine fish. - Source: PubMed
Publication date: 2026/08/05
Ma ChangboZhao WenliBao YangguangYang QiutingWu LiwenZhu TingtingSun PengZhou QicunJin Min - Kashin-Beck disease (KBD) is a chronic, endemic osteoarticular disorder associated with T-2 toxin exposure, which is rapidly metabolized to HT-2 toxin in vivo. However, the role of zinc transporter ZIP6 in HT-2 toxin-induced extracellular matrix metabolic disturbance in chondrocytes remains unclear. This study established HT-2 toxin intervention and ZIP6 knockdown chondrocyte models, combined with quantitative reverse transcription polymerase chain reaction (qRT-PCR) and transcriptome sequencing, to investigate the regulatory mechanisms of ZIP6 in chondrocyte injury. Following HT-2 toxin exposure, altered chondrocyte morphology and reduced cell viability were observed; ZIP6, COL2A1, MTF1, and MTF2 expression were significantly downregulated, whereas MMP1, MMP13, and COL10A1 were upregulated. ZIP6 knockdown significantly upregulated COL2A1, MTF1, and MTF2, downregulated MMP1 and COL10A1, but did not alter MMP13 expression. Differentially expressed genes following ZIP6 knockdown were predominantly enriched in FoxO, cAMP, and TNF signaling pathways. qRT-PCR validation confirmed consistent expression changes in FOXO4, TNFSF10, COLEC10, UCA1, and LRRC17 with transcriptome sequencing results. Collectively, HT-2 toxin suppresses ZIP6, MTF1, and MTF2 expression, disrupting chondrocyte extracellular matrix metabolism; conversely, ZIP6 knockdown ameliorates matrix metabolic abnormalities through modulation of relevant signaling pathways. These findings reveal differential regulatory effects of HT-2 toxin and ZIP6 on cartilage matrix metabolism, providing experimental evidence for elucidating molecular mechanisms underlying cartilage injury-related diseases. - Source: PubMed
Liu YangZhang YuHuang RuitianBai LuluLiu LianWang ChaoweiQin YirongWang HuiGuo XiongWang XiNing Yujie - (1) Background: Reactive oxygen species (ROS) act as physiological signaling mediators but contribute to oxidative damage, cellular dysfunction, and age-related disease when redox homeostasis fails. Forkhead box O4 (FOXO4) has emerged as a redox-sensitive regulator linking stress adaptation, antioxidant defense, and cellular senescence. This structured narrative review critically evaluates which redox- and aging-related conclusions are supported directly for FOXO4 and which remain inferred from other FOXO isoforms. (2) Methods: PubMed/MEDLINE, Scopus, and Web of Science were searched from inception to May 2026; Google Scholar was used only for supplementary citation tracking and did not contribute a separate platform-level count. Of 420 records, 300 remained after deduplication, 110 full texts were assessed, and 89 publications were retained. FOXO4-related evidence was classified as directly FOXO4-specific ( = 18), FOXO-family/conserved ( = 24), or extrapolated predominantly from FOXO1/FOXO3/DAF-16 ( = 20); 27 contextual publications on redox biology, senescence, disease, and NRF2 were tracked separately. (3) Results: The strongest FOXO4-specific evidence supports three mechanistic axes: cysteine-dependent redox sensing, stress-regulated nuclear trafficking and coactivator engagement through transportin-1 and p300/CBP, and FOXO4-p53-mediated survival of senescent cells. By contrast, direct FOXO4 regulation of commonly cited antioxidant targets, including SOD2, catalase, sestrins, and GADD45, remains insufficiently demonstrated and is inferred mainly from FOXO3 or broader FOXO-family studies. FOXO4-DRI has shown senolytic activity in preclinical models, including vascular endothelium, but has not been clinically validated. (4) Conclusions: FOXO4 is a redox-responsive transcriptional regulator with well-supported roles in cysteine-based signaling and senescent-cell survival, whereas its target-gene-level antioxidant program remains incompletely resolved. Clinical translation of FOXO4-p53 disruption requires isoform- and tissue-specific validation, pharmacokinetic and delivery studies, long-term toxicology, and explicit assessment of p53-dependent tumor surveillance. - Source: PubMed
Publication date: 2026/07/03
Mateescu Diana-MariaGavrilescu Dragos-MihaiMarinescu Adelina-RalucaRosca OvidiuLazureanu Voichita ElenaIlie Adrian-CosminMuresan Camelia-OanaEnache Alexandra