FOXO3A (DN)
- Known as:
- FOXO3A (DN)
- Catalog number:
- 000422A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FOXO3A ()
Related genes to: FOXO3A (DN)
- 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: FOXO3A (DN)
Related articles to: FOXO3A (DN)
- Malignant ovarian germ cell tumors (MOGCTs) predominantly affect children and young women. Cisplatin-based chemotherapy is effective but frequently causes premature ovarian failure (POF). The PI3K/AKT pathway drives both MOGCT pathogenesis and chemotherapy-induced ovarian damage, yet no strategy simultaneously targets both. This study investigates whether the selective PI3Kγ inhibitor eganelisib can exert dual antitumor and ovarian-protective effects by modulating the AKT1-OCT4/SOX2 axis. - Source: PubMed
Publication date: 2026/06/13
Xu YanningYi LiLiu JinzhuChen QuanyuJi YijieLiu BingbingLi HanboGong XueLiu WenbiaoLi ShuangshuangShen XinghuiChen Ling - Circular RNAs (circRNAs) are important regulators of signaling pathways involved in intervertebral disc degeneration (IVDD). This study investigated the role and underlying mechanism of circTMEM230 in the degeneration of endplate chondrocytes. We observed that circTMEM230 expression was significantly downregulated in chondrocytes subjected to intermittent cyclic mechanical tension (ICMT). Functional assays demonstrated that overexpression of circTMEM230 enhanced the expression of extracellular matrix (ECM)-related genes through modulation of the miR-223-3p/FOXO3/SOX9 signaling axis. Specifically, circTMEM230 acted as a molecular sponge for miR-223-3p, thereby upregulating FOXO3, which subsequently promoted SOX9 transcription. In vivo experiments further confirmed that circTMEM230 mitigated IVDD progression and regulated the expression of miR-223-3p, FOXO3, and SOX9. Additionally, expression levels of circTMEM230, miR-223-3p, FOXO3, and SOX9 were found to be correlated in endplate cartilage tissue samples from IVDD patients. These findings suggest that circTMEM230 exerts a protective role in IVDD and may serve as a promising therapeutic target for further investigation. - Source: PubMed
Zheng QuanYang JiongLi Xing-XingShao SongWang Chuan-DongWang Qi-WeiSun Liang-Ye - Hydroxysafflor Yellow A (HSYA), the major bioactive component from L., exerts significant protective effects against myocardial ischemia-reperfusion injury (MIRI). Mitophagy is pivotal in the pathological process of MIRI, yet the specific molecular mechanism underlying HSYA-mediated mitophagy regulation remains unclear. - Source: PubMed
Publication date: 2026/05/31
Meng DongdongXia WencongTian FengHuang QiGe ChaowenWang Ning - Oxidative stress causes brain damage contributing to neurodegenerative and vascular diseases. In Alzheimer's disease (AD), elevated oxidative stress and mitochondrial damage are closely linked to misfolded protein accumulation. ROS also plays a major role in ischemic brain injury, particularly during reperfusion, impairing the blood-brain barrier and highlighting the association between vascular pathology and AD. To investigate perturbations in brain cells occurring in mixed dementia (AD combined with vascular dementia components), we used a triple culture system comprising neurons, astrocytes, and microglia and induced neuronal injury by combining LPS and HO exposures. Cell viability assays revealed that neuronal death occurred mainly through apoptosis and DNA damage. In neurons and astrocytes exposed to LPS+HO, the expression of NADPH oxidase isoform 2, a major source of ROS, increased, along with FOXO3 and SOD2, a key mitochondrial ROS scavenger. Indeed, these changes were accompanied by altered mitochondrial morphology and integrity, as well as reduced neurite extension and thickness. The treatment with extracellular vesicles (EVs) derived from amniotic fluid stem cells was tested due to their rich content of antioxidant molecules. Interestingly, EVs reversed the negative effects of LPS+HO, suggesting the protective role against neuronal injury in vitro may be mediated by the EV-cargo. - Source: PubMed
Publication date: 2026/05/27
Malenchini MartaBeretti FrancescaGatti MartinaBertucci EmmaDel Toro ElenaMaraldi Tullia - Pathological remodeling after myocardial infarction (MI) involves multifactorial mechanisms, highlighting the need for combinatorial therapeutic strategies. Synthetic mRNAs offer design flexibility and represent a modality particularly suitable for such approaches. To investigate this, five genes (, , , , and ) were selected from a model in which extracellular vesicles secreted by human iPSC-derived cardiomyocytes restored cardiac function. Synthetic mRNAs encoding these genes were delivered via polyplex nanomicelles by direct myocardial administration in mice with MI-induced heart failure. Nanomicelles have been shown to provide stable encapsulation, enhanced local expression, and prolonged persistence. This treatment promoted angiogenesis via the PI3K-Akt-ETV4 axis, suppressed fibrosis via inhibition of the JNK/FOXO3 pathway, and enhanced repair by activating ERK signaling, together yielding multifaceted benefits, including tissue regeneration, improved contractility, and extended survival. These findings establish the therapeutic potential of multigene mRNA cocktail therapy for post-MI heart failure and mark an important step toward developing new interventions for diseases characterized by complex remodeling. - Source: PubMed
Publication date: 2026/05/23
Handa KazumaKawamura TakujiMano YasunobuNakanishi HideyukiFujimura LisaKawai ChieHarada AkimaTorigata KosukeMiki KenjiItaka KeijiMiyagawa Shigeru