FOXO6 Antibody (Center)
- Known as:
- FOXO6 Antibody (Center)
- Catalog number:
- AP12340c
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- FOXO6 Antibody (Center)
Related genes to: FOXO6 Antibody (Center)
- Gene:
- FOXO6 NIH gene
- Name:
- forkhead box O6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-04-10
- Date modifiied:
- 2018-11-15
Related products to: FOXO6 Antibody (Center)
Related articles to: FOXO6 Antibody (Center)
- FOXO6 is a member of the FOXO transcription factor family that differs from FOXO1, FOXO3, and FOXO4 in its nucleocytoplasmic regulation, remaining predominantly within the nucleus because it lacks a functional nuclear export sequence. FOXO6 activity can nevertheless be inhibited by insulin/AKT signaling, whereas impaired insulin signaling increases its transcriptional activity in hepatocytes under insulin-resistant and nutrient-rich conditions. Recent studies indicate that FOXO6 regulates hepatic metabolic pathways associated with oxidative injury, inflammatory signaling, and lipid accumulation. In hepatocellular carcinoma, increased FOXO6 expression is associated with glycolytic activity, proliferation, and invasion. We recently reported that FOXO6-dependent transcriptional regulation contributes to reactive oxygen species (ROS) production and inflammasome-associated inflammatory signaling through induction of thioredoxin-interacting protein (TXNIP). Furthermore, FOXO6 regulates lipid metabolic pathways through transcriptional activation of apolipoprotein C3 (ApoC3) and peroxisome proliferator-activated receptor (PPAR) γ together with suppression of PPARα, thereby promoting triglyceride accumulation, mitochondrial dysfunction, and lipotoxic injury in hepatocytes. These metabolic and inflammatory alterations contribute to hepatic steatosis, mitochondrial injury, and inflammatory hepatocellular damage. In hepatocellular carcinoma, increased FOXO6 expression is associated with glycolytic metabolism, angiogenic signaling, proliferative activity, immune suppression, and invasive phenotypes. FOXO6-dependent signaling interacts with STAT3, NF-κB, and β-catenin pathways involved in metabolic adaptation and tumor progression. Recent studies demonstrate relationships between increased FOXO6 expression, vascular invasion, aggressive tumor phenotypes, and reduced survival in hepatocellular carcinoma. This review examines FOXO6-associated transcriptional mechanisms involved in hepatic metabolic inflammation and hepatocarcinogenesis. - Source: PubMed
Kim Mi EunKim YukyeongLee Jun Sik - - Source: PubMed
Publication date: 2026/08/27
Miao JinhuaLi JiemeiMeng PingLi XiaolongHuang JiewuLiang YeLing XianWang XiaoxuShen WeiweiZhou ShanPeng HongquanZhang YunfangLiu YouhuaHou Fan FanZhou Lili - Diabetic retinopathy (DR) is the main cause of vision loss, with retinal pigment epithelial (RPE) cell dysfunction as a key contributor. Ferroptosis is implicated in RPE injury under hyperglycemia; however, its upstream regulatory mechanisms remain unclear. High glucose (HG)-induced human RPE ARPE-19 cells and a diabetic mouse model were used. Ferroptosis was assessed through biochemical assays, Western blot, fluorescence probes, and histological staining. Protein interactions and transcriptional regulation were examined using Co-IP, glutathione S-transferase pull-down, ChIP, and luciferase reporter assays. Immunofluorescence staining was used as key indicator expression in retinal tissues. Nuclear receptor 4A1 (NR4A1) expression was upregulated under HG-induced ARPE-19 cells. NR4A1 knockdown alleviated HG-induced iron accumulation, lipid peroxidation, and ferroptosis marker changes. Mechanistically, SMAD-specific E3 ubiquitin protein ligase 2 (SMURF2) interacted with NR4A1 and promoted its ubiquitination and degradation. Forkhead box O6 (FOXO6) was upregulated by HG and repressed SMURF2 transcription. SMURF2 overexpression mitigated HG-induced ARPE-19 ferroptosis and retinal injury in DR mice, an effect reversed by NR4A1 co-overexpression. SMURF2 knockdown reversed the effect of FOXO6 knockdown on HG-induced ferroptosis in ARPE-19 cells and retinal injury in DR mice. The FOXO6-SMURF2-NR4A1 axis critically regulates ferroptosis in RPE cells during DR. - Source: PubMed
Publication date: 2026/08/26
Chen QiaoSu BoXu KeLi LiangChen Changzheng - Butyl benzyl phthalate (BBP), a widely used endocrine-disrupting chemical, has been associated with reproductive toxicity; however, its long-term effects during aging remain poorly understood. In the present study, we examined the effects of prolonged BBP exposure on the male reproductive system using naturally aged C57BL/6J mice. Mice received BBP at 169 μg/kg/day in drinking water for 10 or 22 months and were analyzed at 24 months of age. No significant differences in body weight, food intake, or water consumption were observed among the experimental groups. Representative gross images showed apparent distension and dark-red discoloration of the seminal vesicles in BBP-exposed aged mice. Compared with Young mice, the BBP-exposed aged groups showed higher expression of IL-1β, IL-6, TNFα, SOD1, and SOD2 and lower CAT expression in the seminal vesicle. HDCFDA fluorescence showed a non-significant increasing trend. Because an untreated age-matched Old group was not included in the seminal vesicle analyses, the effects of aging and BBP could not be distinguished. In contrast, the testis showed limited changes in inflammatory cytokine-, antioxidant enzyme-, and steroidogenesis-related gene expression and in HDCFDA fluorescence relative to the untreated Old group. Exploratory miRNA sequencing of pooled testicular RNA and comparison with a TM3 Leydig cell dataset identified miR-664-5p as a candidate showing higher relative abundance in both datasets. TargetScan analysis predicted binding sites for miR-664-5p in FOXO1 and FOXO3. In BBP-treated TM3 cells, FOXO3 protein expression was decreased, and FOXO6 expression was increased, whereas FOXO1 showed no consistent dose-dependent change. These molecular findings do not establish direct regulation of FOXO proteins by miR-664-5p or explain the seminal vesicle findings. - Source: PubMed
Publication date: 2026/08/17
Hwang SeonhwaKang Hyun BonKim Dae HyunKim Hyung HoiPark Min Hi - - Source: PubMed
Publication date: 2026/08/21
Nichols Meredith MAlruwaii FatimahChaaban Mohamad RCheng Yu-WeiGriffith Christopher C