Ask about this productRelated genes to: FOXO6 Blocking Peptide
- 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 Blocking Peptide
Related articles to: FOXO6 Blocking Peptide
- Abnormal cell fate transition determines cell instability, which can contribute to disease development. In chronic kidney disease, many renal tubular cells exhibit senescent phenotypes. The fundamental mechanisms of this fate transition remain undetermined. Here we discover that WNT10B, a ligand of the Wnt family, accelerates CKD progression through tubular senescence and proinflammatory microenvironments. Mechanistically, WNT10B mediates metabolic reprogramming from fatty acid oxidation to glycolysis, thus promoting cell senescence and cytokine secretion. Genetic ablation of Wnt10b in male CKD mouse model effectively inhibits cell senescence, inflammation, and fibrogenesis by maintaining metabolic homeostasis. Conversely, Wnt10b transgene in tubular cells aggravates metabolic imbalance, and promotes tubular senescence and fibrogenesis. Forkhead box O6 (FOXO6), a DNA-binding transcription factor, mediates the signal transduction cascade of WNT10B. ChIP-, bulk RNA-, and single-nucleus RNA- sequencing and biological assays verify that FOXO6 transcriptionally modulates PPARA and PKM to control metabolic reprogramming and regulate senescence fate transition in tubular cells. Therefore, the study reveals that WNT10B/FOXO6 signaling controls tubular cell senescence fate, and sheds a light on potential intervention targets to protect against CKD. - Source: PubMed
Publication date: 2026/04/10
Miao JinhuaLi JiemeiMeng PingLi XiaolongHuang JiewuLiang YeLing XianWang XiaoxuShen WeiweiZhou ShanPeng HongquanZhang YunfangLiu YouhuaHou Fan FanZhou Lili - Escalating surface ultraviolet-B (UVB) radiation accelerates skin photoaging and underscores the need for safe, plant-derived photoprotectants. Amentoflavone (AF), the principal biflavonoid of the resurrection plant Selaginella tamariscina, has recognized anti-photoaging activity, yet its epidermal mechanism remains undefined. This study utilized animal and cellular models to investigate the therapeutic potential of AF (0.1-0.2 mg g) against photoaging. AF restored skin hydration and elasticity, reduced melanin deposition, and reversed UVB-induced epidermal hyperplasia and collagen/elastic-fiber disorganisation. AF decreased ROS and MDA while normalizing SOD, CAT and GSH-Px activities. Docking (LibDockScore = 125.596) and microscale thermophoresis (MST) revealed high-affinity AF-PAR2 interaction. Treatment with AF reduced PAR2 and Gαq levels, curtailed activation of PI3K, phosphorylated Akt, and phosphorylated FoxO6, and restored FoxO6 nuclear localization, which in turn enhanced MnSOD and CAT expression. In addition, AF suppressed UVB-induced upregulation of senescence-associated markers p16, p21, and GLB1 in both rat skin and HaCaT cells. However, administration of the PAR2 agonist SLIGRL-NH negated these benefits in both cellular and animal models. These findings position AF as a promising natural agent for anti-photoaging dermotherapy and provide a mechanistic basis for S. tamariscina-based product development. - Source: PubMed
Publication date: 2026/04/09
Li LinLi ZhiweiXiao ShanLi AngTian FangShu PengGu Wei - Autophagy genes are essential for proper uterine function, reproductive physiology, and the maintenance of endometrial atrophy (EA). - Source: PubMed
Aslanian-Kalkhoran LidaSoltani-Zangbar Mohammad SadeghAghebati-Maleki AliAhmadpourYoushanlui MahyaYousefi MehdiAghebati Maleki Leili - Population admixture is a potent evolutionary force shaping genomic diversity, yet its influence on the dynamics and functional consequences of structural variation (SV) remains poorly understood. Here, we present a comprehensive whole-genome sequencing analysis of SVs in the Uyghurs, a model admixed Eurasian population with distinct Western and Eastern ancestral contributions. We identified 9965 high-confidence SVs, revealing that Uyghurs exhibit 32% novel SVs and 1.19-fold greater SV-transcription diversity compared to their ancestral source populations. Crucially, SV diversity follows a non-linear parabolic relationship with ancestry proportions (r = 0.94), peaking when Western/Eastern ancestry contributions are balanced. Admixture-induced recombination at ancestry junctions creates SV hotspots via non-allelic homologous recombination (NAHR), with 60% of post-admixture SVs flanked by homologous repeats. Ancestry-divergent SVs disproportionately regulate gene expression, while admixed variant combinations (e.g. and loci) disrupt immune/metabolic pathways via additive regulatory effects. Strikingly, while Uyghurs harbor elevated SV diversity, the burden of pathogenic variants remains comparable to ancestral populations, suggesting buffering mechanisms against genetic load. Evolutionarily, younger SVs tend to be larger in size, exert stronger regulatory impacts and exhibit higher predicted pathogenicity. These findings establish admixture as a dual force of genomic diversification and functional equilibrium, bridging evolutionary dynamics with biomedical insights. Our work underscores the necessity of SV-aware approaches in genetic medicine and highlights how admixed populations broaden genomic diversity beyond ancestral boundaries through novel variant combinations. - Source: PubMed
Publication date: 2025/11/21
Lou HaiyiWang YiminChai YuNing ZhilinFu RuiqingLu YanXie BoMa SenPan YuwenGao YangLu DongshengBai XinyueYang YajunMamatyusupu DolikunXu Shuhua - Aging contributes to hepatic steatosis by increasing de novo lipogenesis. The Forkhead box O6 (FOXO6) transcription factor links insulin signaling to lipid metabolism. Activated FOXO6 induces hyperlipidemia and decreases peroxisome proliferator-activated receptor alpha (PPARα), thereby promoting hepatic lipogenesis. In this paper, we describe the role of FOXO6 in hepatic steatosis in aged male rats and liver cells, and examine the relationship between FOXO6 and PPARα, and the functional consequences of their altered interaction. We find that FOXO6 induces lipid accumulation by inhibiting PPARα in aged male rat livers. Our data show that AKT signaling negatively regulates FOXO6-induced hepatic lipid accumulation, and that a key β-oxidation gene, PPARα, is decreased in aged livers. We further demonstrate that FOXO6 activation decreases PPARα expression and increases lipid accumulation. Furthermore, interaction between FOXO6 and PPARα promotes hepatic steatosis in aged males. Also, high glucose upregulates Foxo6, reduces β-oxidation gene expression, and increases cellular TG-mediated lipid accumulation. Transcriptional activation of FOXO6 by aging and high glucose cause lipid accumulation by downregulating PPARα and hyperglycemia-responsive genes in aged male rats and liver cell cultures. We provide evidence that age-related insulin resistance suppresses β-oxidation through interaction between FOXO6 and PPARα, thereby promoting hepatic lipid accumulation in aged male rats. - Source: PubMed
Publication date: 2026/02/09
Kim Yeong UnPark Ji HyunKim Dae Hyun