FOXO3 (phospho-Ser253) Antibody
- Known as:
- FOXO3 (phosphorilated-Ser253) Antibody
- Catalog number:
- abx000399
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- FOXO3 (phospho-Ser253) Antibody
Related genes to: FOXO3 (phospho-Ser253) Antibody
- 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: FOXO3 (phospho-Ser253) Antibody
Related articles to: FOXO3 (phospho-Ser253) Antibody
- As a common clinical syndrome with high morbidity and mortality, acute kidney injury (AKI) involves epigenetic mechanisms that remain largely uncharacterized. In this study, we identify a previously uncharacterized long non-coding RNA mmu-lncR-gm33782 and its human homolog hsa-lncR-CLLU1-AS1 as a critical epigenetic driver of AKI. We found that LncR-gm33782 was markedly upregulated in AKI kidneys, and its genetic ablation substantially alleviated tubular injury and inflammation. Transcriptomic profiling revealed that lncR-gm33782 overexpression broadly upregulated genes encoding components of the PA1-MLL3/4 methyltransferase complex. Mechanistically, lncR-gm33782 functionally engages the PAXIP1 associated glutamate rich protein 1 (PA1) promoter to enhance PA1 transcription. Elevated PA1 facilitated recruitment of the Lysine methyltransferase 2C and lysine methyltransferase 2D (MLL3/MLL4) complex to an intronic enhancer within the Forkhead box O3 (Foxo3) locus, leading to increased histone H3 lysine 4 monomethylation (H3K4me1) and histone H3 lysine 27 acetylation (H3K27ac) deposition. Consequently, Foxo3 expression was activated and established a positive autoregulatory loop that further amplified its expression. In vivo, locked nucleic acid modified antisense oligonucleotide (ASO) mediated knockdown attenuated AKI induced renal injury while concomitantly suppressing PA1 and Foxo3 expression. Notably, the human homolog hsa-lncR-CLLU1-AS1 was consistently upregulated in the blood of AKI patients and positively associated with serum creatinine as well as blood urea nitrogen. Our findings uncover a conserved lncRNA-PA1-MLL3/4-Foxo3 epigenetic axis that drives enhancer reprogramming and a self-reinforcing Foxo3 circuit. These findings position this lncRNA as a promising therapeutic target and its human homolog as a circulating biomarker for AKI. - Source: PubMed
Publication date: 2026/09/11
Tan Rui-ZhiJia JianBai Qiu-XiangLi TongWang Hong-LianLei Xian-YingShu JingMao NanKantawong FahsaiWang Li - Apoptosis and functional loss of articular chondrocytes serve as initiating events in temporomandibular joint osteoarthritis (TMJOA), and FoxO3 represents a critical molecule for sustaining chondrocyte homeostasis. This study investigates the regulatory mechanism of the lncRNA-OIP5-AS1/hsa-miRNA-223-3p/FoxO3 axis in TMJOA, aiming to identify potential therapeutic targets for this disease. Single-cell database analysis first revealed markedly reduced FoxO3 expression in TMJOA-derived chondrocytes. A rat TMJOA model was then constructed and assigned to control, model, and FoxO3 overexpression groups; micro-CT and histological staining, including HE and Safranin O-fast green staining, were applied to assess articular cartilage injury, while immunohistochemistry was used to detect cartilage-associated proteins Col2a1, MMP-13, Aggrecan, and ADAMTS-5. Further in vitro experiments validated the chondroprotective function of FoxO3 as well as the binding interaction between FoxO3 and rno-miRNA-223-3p. Database screening confirmed significant down-regulation of FoxO3 in TMJOA cartilage. Animal experiments demonstrated that FoxO3 overexpression mitigated chondrocyte injury in rat TMJOA lesions, increased Col2a1 and Aggrecan levels, and suppressed MMP-13 and ADAMTS-5 expression. Cellular assays showed that FoxO3 overexpression enhanced chondrocyte proliferation and matrix synthesis and preserved chondrocyte function. Sequencing and cellular evidence indicated that rno-miRNA-223-3p directly targets FoxO3 mRNA to repress its transcription and negatively modulate FoxO3 abundance, consequently aggravating chondrocyte apoptosis. Collectively, rno-miRNA-223-3p suppresses FoxO3 activity to facilitate TMJOA pathogenesis, and the lncRNA-OIP5-AS1/rno-miRNA-223-3p/FoxO3 regulatory cascade may act as a promising molecular target for TMJOA clinical intervention. - Source: PubMed
Xu XuesongQiao Shichong - Grip strength has emerged as one of the most robust predictors of mortality, disability and healthspan across populations. Yet its predictive validity rests on an often-unstated assumption: that grip strength serves as a passive readout of systemic biological integrity rather than an isolated measure of forearm function. Here we propose that grip strength derives its prognostic power from its position as a convergent output of multiple aging-sensitive physiological systems-including neuromuscular, vascular, metabolic, endocrine and inflammatory networks. We highlight the neuromuscular junction (NMJ) as a particularly critical and often-overlooked rate-limiting factor, noting that age-related strength loss (∼2.5-4% annually) outpaces mass loss (∼0.6-1% annually) by two-to fivefold-a disparity attributable in large part to NMJ deterioration. We introduce the concept of biomarker decoupling and apply it to the emerging landscape of longevity gene therapies being explored in early translational and compassionate-use settings-including follistatin, klotho, FOXO3, hTERT, SIRT1, PGC-1α, VEGF and FGF21. Critically, we argue that follistatin's anabolic efficacy is contingent on intact NMJ integrity, with denervated muscle fibers exhibiting a blunted net anabolic response despite elevated follistatin expression-creating a therapeutic paradox wherein mass gains can occur without proportional functional improvement. We provide a conceptual analysis of how each therapy may influence grip strength, predict decoupling risk based on the breadth of systems affected, outline plausible timing windows for intervention, and propose a heuristic framework for clinical interpretation. The decoupling categories and any numeric ranges presented here are conceptual and hypothesis-generating rather than empirically validated. - Source: PubMed
Publication date: 2026/08/27
Sewell Patrick EJensen Christopher - Cinnamic acid (CA), a natural phenolic compound with antioxidant and anti-inflammatory properties, has recently attracted attention for its potential protective effects on liver function. This study aimed to evaluate the hepatoprotective effects of CA against carbon tetrachloride (CCl₄)-induced toxicity in mice. - Source: PubMed
Publication date: 2026/09/04
Nomiri SamiraTaebi ReyhanehMohammadi YaserYousefi ToobaAsgari FatemehYazdanimoghaddam FarzanehMortazavi NafisehAmini Abdollah - Age-related fertility decline is an increasingly important challenge in reproductive medicine, driven largely by progressive ovarian aging. The aging ovary undergoes functional deterioration characterized by reduced ovarian reserve and declining oocyte quality, ultimately limiting female reproductive lifespan. Although multiple molecular and cellular processes associated with ovarian aging have been identified, these mechanisms are often discussed independently, limiting an integrated understanding of how they interact within the ovary. In this review, we propose an ovary-centered, multi-mechanistic framework to organize current evidence on ovarian aging and fertility decline. We discuss how genomic instability, telomere attrition, mitochondrial dysfunction, oxidative stress, chronic cellular stress responses, and alterations in ovarian signaling and microenvironmental homeostasis collectively contribute to follicle depletion and impaired oocyte competence. Particular emphasis is placed on signaling pathways involved in follicle activation and stress adaptation, including PI3K/AKT/mTOR, FOXO3, Hippo, and AMPK-Sirtuin networks, while acknowledging that many mechanistic relationships remain incompletely defined in physiological ovarian aging. Building on this integrative perspective, we further evaluate mechanism-oriented intervention strategies, including mitigation of cellular stress, metabolic and signaling modulation, optimization of the ovarian microenvironment, established fertility preservation technologies, and emerging exploratory approaches. By integrating current mechanistic and translational evidence, this review provides a conceptual framework for understanding ovarian aging and highlights future directions for evidence-based fertility preservation and reproductive health management in the context of aging. - Source: PubMed
Publication date: 2026/08/04
Chen JianhuiDuan XiaohuiJing YalingLiu XiaofangZhang YongqiangTang YuqinChen ChuanliangYang JiayanLi XiaohongLin FangZhao Lianfang