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
- Conventional tobacco use causes a wealth of diseases and adversely affects cells and organ systems across the body. The long-term effects of e-cigarette vaping on the same remain unclear. Identifying early pathogenic signals at the organ level via animal models may shed light on potential downstream effects in humans. Here we investigate transcriptomic changes in the kidney and liver, organs known to be damaged by long-term combustible tobacco use, of mice exposed daily to e-cigarette aerosols (vapor) with or without nicotine. C57BL/6 male 6-8 week-old mice underwent whole-body exposure to room air, e-cigarette (3rd generation box mod) vapor containing 70:30 propylene glycol and glycerin (PG: Gly) without nicotine (Vehicle), and e-cigarette vapor with 6 mg/mL freebase nicotine in 70:30 PG: Gly (E-cig) for 1 h daily for 3 months. RNA sequencing on kidney and liver tissues and apriori gene set analysis were performed. Unbiased principal component analysis identified closer clustering of E-cig and Vehicle groups, relative to Air, in the kidney. Assessment of the a priori gene set found nicotine to be associated with greater transcriptomic changes in the kidney while vehicle chemicals induced greater changes in the liver. Alterations in expression of Car3 and Foxo3 identify oxidative stress and inflammation in the renal system associated with e-cigarette exposure, while dysregulated Il6ra and Lpin1 in the liver highlight disruptions in lipid metabolism and immune signaling. Chronic inhalation of e-cigarette vapor alters gene expression in downstream organs, in a pattern most consistent with promotion of fibrosis and metabolic dysregulation, underscoring the need to define long-term pathophysiologic effects of e-cigarette vaping across the body. - Source: PubMed
Publication date: 2026/07/31
Gu WanjunChang HowardSaini PoorviGaboyan SamvelOlay JarodMasso-Silva Jorge AShin JohnAdvani IraDu AshleyBrand CameronHeller Brown JoanPerryman AlexiaCrotty Alexander Laura E - A common cause of multidrug-resistant (MDR) cancer is imbalanced redox signaling, which reduces the effectiveness of chemotherapy and promotes regrowth of cancer cells. Amplification of thioredoxin reductase (TrxR) and activation of the Keap1-Nrf2-FOXO3 pathway may contribute to enhanced drug efflux, strengthens antioxidant defenses, and resistance to oxidative stress-induced apoptosis in certain tumors. Redox-based drug repurposing offers a promising strategy to overcome MDR by targeting these shortcomings. Repurposing drugs including metformin, auranofin, brusatol, and natural polyphenols increase reactive oxygen species (ROS) and make MDR cells more sensitive to chemotherapy via modulation and inhibiting Nrf2 or TrxR. Nanotechnology advancements and combination of repurposed drugs with anticancer drugs, ferroptosis inducers may improve tumor selectivity while lowering systemic toxicity. Preclinical experiments show effectiveness by suppressing antioxidant pathways, inhibiting efflux pump function, and delivering drugs in a redox-responsive manner. Next-generation tumor-selective delivery systems, adaptive clinical trial designs, and biomarker-driven patient classification based on TrxR expression or Keap1/Nrf2 mutations are the main areas of focus. Translation into clinical practice could be accelerated by combining specific redox profiling, nanocarrier technologies, and pharmacokinetics. For MDR cancer, redox-targeted drug repurposing is an effective, precision-based strategy for recovering chemosensitivity and enhancing treatment outcomes. - Source: PubMed
Pawar Charan SinghPrasad Nagarajan Rajendra - Climate-induced heat stress poses a major challenge to small ruminant productivity in arid and semi-arid regions, affecting growth, metabolism, and immune function. This study examined tissue-specific molecular responses to chronic heat stress in lambs by evaluating the expression of key genes associated with inflammation, oxidative stress, proteostasis, and muscle function in the liver and skeletal muscle. Twenty-four lambs were reared at two climatically contrasting field sites (thermoneutral vs. high-THI) for 42 days. In the liver, exposure to the heat-stressed environment was associated with decreased SOD1 expression alongside increased FOXO3 and pro-inflammatory IL-6, while TNF-α and PPARγ were significantly lower. In muscle, a different profile emerged: heat shock proteins (HSP70, HSP90) and the apoptotic marker CASP3 were strongly upregulated, MYOD was suppressed, and ACTB3 remained stable. These results suggest candidate tissue-specific transcriptional signatures associated with impaired muscle regeneration and enhanced proteotoxic stress, although the field-based design confounds thermal load with other site-specific factors and does not permit causal attribution. Composite gene expression ratios-such as SOD1/IL-6 and FOXO3/TNF-α-were elevated under heat stress and negatively correlated with rectal temperature, indicating a potential role as candidate molecular indices associated with thermal response. Principal component analysis further distinguished control and heat-stressed animals based on transcriptional profiles. These findings highlight the coordinated yet divergent molecular strategies employed by liver and muscle tissues under prolonged thermal stress. The study provides preliminary, hypothesis-generating insight into gene-level responses associated with contrasting thermal environments and identifies candidate molecular targets warranting further validation in controlled designs before application to selection or intervention strategies. - Source: PubMed
Publication date: 2026/07/28
Alrhaif Rafid Hafedh SabeehAhmadpour AmirZarrin Mousa - Cashmere production declines with age in cashmere goats, but the molecular mechanisms are unknown. This study employed a transcriptome-wide RNA-seq analysis to compare age-associated and breed-related gene expression profiles in goat skin, with particular emphasis on age-dependent expression and its associated signaling pathways. Skin tissues from cashmere goats at 12 and 15 months and age-matched non-cashmere controls were analyzed by RNA-seq (BGIDNBSEQ platform). Differential expression and functional enrichment analyses were performed on skin transcriptomes of cashmere and control goats at 12 and 15 months. Age-specific functional profiles emerged: 12-month cashmere goats showed enrichment in GTPase activity, glucose transport, and ribosomal assembly, whereas 15-month goats were enriched for autophagosome assembly and apoptosis. FoxO signaling was commonly enriched across both ages, while the Hepatitis B pathway was unique to 12 months. was significantly upregulated at 12 months coinciding with peak cashmere production with reduced expression at 15 months. This age-dependent pattern was supported by coordinated regulation of downstream effectors, including , , , and . Collectively, these transcriptomic data provide a mechanistic framework linking age-dependent regulation to the decline in cashmere fiber production. - Source: PubMed
Publication date: 2026/07/10
Ghauri Muhammad ZainZafar AyeshaNiaz M KhuzemaNazir UsmanMunir AsimHamza MuhammadZahra KiranJi Dejun - : Mitochondrial bioenergetic dysregulation disrupts immune-metabolic homeostasis and promotes pro-inflammatory microenvironments in osteoarthritis (OA) synovitis. However, the mechanistic contributions of mitochondrial energy metabolism to synovitis pathogenesis in OA remain poorly defined. : We analyzed mitochondrial energy metabolism-related genes () in OA synovitis by integrating transcriptomic data from OA synovial tissues (GSE55235, GSE55457). LASSO regression and maximal clique centrality (MCC) algorithms were applied to identify hub genes, and single-cell RNA sequencing (GSE152805) was used to examine cell-type-specific expression patterns. Functional validation was performed in IRS2-knockdown THP-1 macrophages. : We identified 22 mitochondrial energy metabolism-related differentially expressed genes (MEMR-DEGs), which were enriched in the AMPK signaling, glucagon signaling, and insulin signaling pathways. Four hub genes (, , , ) were identified, and their expression was negatively correlated with synovial macrophage infiltration. Single-cell RNA sequencing revealed that was specifically upregulated in a synovial macrophage cluster. Functional studies in IRS2-knockdown THP-1 macrophages demonstrated that IRS2 deficiency impaired IL-4-induced M2 macrophage polarization and reduced mitochondrial membrane potential and ATP synthesis, which was mediated by the suppression of the AKT/FOXO1 signaling. : IRS2 potentially influences mitochondrial energy metabolism, as evidenced by the maintenance of mitochondrial membrane potential and ATP synthesis, via the AKT/FOXO1 signaling pathways to maintain synovial macrophage M2 polarization homeostasis. These findings provide novel molecular targets for addressing immune-metabolic pathways in OA therapy. - Source: PubMed
Publication date: 2026/06/30
Yang YunlongZhang NianlongLi XuyangXie EnbeiWu YangyuZhou Jianlin