FOXO6 Blocking Peptide, Blocking Peptides
- Known as:
- FOXO6 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-4687
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- FOXO6 Blocking Peptide Peptides
Related genes to: FOXO6 Blocking Peptide, Blocking Peptides
- 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, Blocking Peptides
Related articles to: FOXO6 Blocking Peptide, Blocking Peptides
- 1. The following study investigated the regulation of Intramuscular fat (IMF) deposition at different developmental stages in Jingyuan chickens. Pectoral muscles from hens at 42, 126 and 180 days of age were analysed using transcriptome sequencing and weighted gene co‑expression network analysis (WGCNA).2. A total of 1187, 1377 and 617 differentially expressed genes (DEGs) were identified in the three pairwise comparisons, respectively. Among these, , and are known to be involved in IMF synthesis and metabolism through energy and amino acid metabolic pathways.3. The WGCNA data identified three modules (MEyellow, MEbrown, MEdarkred) that were significantly correlated with IMF content and age ( < 0.05). Functional analysis indicated that , and were enriched in both FoxO and GnRH signalling pathways. This suggested potential roles in IMF deposition. Further investigation of DEG and the three modules revealed and as candidate genes that could influence IMF deposition in muscle.4. The data represents a transcriptomic resource for IMF deposition in Jingyuan chicken breast muscle. The results identified candidate genes for future molecular breeding aimed at improving meat quality. - Source: PubMed
Publication date: 2026/07/03
Wang HWang CZhao WYu BHu JZhang JGu Y - Hepatocellular carcinoma (HCC) is a lethal malignancy driven by cancer stem cells, which drive progression and therapeutic resistance. Nuclear pore protein ELYS is implicated in tumorigenesis, but its role in HCC stemness remains unclear. - Source: PubMed
Publication date: 2026/06/02
Chen XinZhang QingXie FenZhai HuilanLi ChuanhongZhou WeifengZhang Nuobei - BackgroundIntegrated bioinformatics approaches were used to identify stage-specific candidate genes and potential drug targets in triple-negative breast cancer (TNBC).MethodsMicroarray (164 early-stage, 33 advanced-stage, and 53 normal samples) and RNA-seq (113 normal, 163 early-stage, and 30 advanced-stage TNBC samples) datasets were analyzed. Differentially expressed genes (DEGs) were identified, followed by co-expression analysis using Weighted Gene Co-expression Network Analysis (WGCNA) and protein-protein interaction analysis using the STRING database. miRNA co-regulation was evaluated using multiMiR and TCGA correlation analyses. Candidate genes were validated using UALCAN and immunohistochemistry data. Molecular docking assessed potential therapeutic agents.ResultsNovel stage-specific candidate biomarkers were identified, including , , , and in early-stage TNBC, and , , , and in advanced-stage TNBC. UALCAN analysis confirmed the dysregulation of these genes across 23 additional malignancies. STRING-based network analysis revealed stage-specific protein-protein interactions, including SKP2-SKP1 in early-stage and F11R-TJP1 in advanced-stage TNBC. miRNA co-regulation distinguished early-stage TNBC through PI3K-AKT-related pathways and advanced-stage TNBC through tumor progression-associated pathways. Docking-based drug repurposing highlighted conventional agents (e.g., doxorubicin) and potential novel candidates (e.g., sunitinib).ConclusionThis study identifies novel stage-specific gene candidates and suggests repurposable drugs for TNBC, supporting progression-specific targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/05/28
Shahraki FaezeMeshkini AzadehNazari Elham - Neurodegenerative diseases (NDDs) lack effective disease-modifying therapies. The FOXO transcription factors serve as integrative hubs of cellular stress responses, operating through cell-autonomous homeostasis, intercellular coordination, intracellular quality control, and cell fate decisions four hierarchical tiers. This review systematically examines isoform-specific functions: FOXO1 governs metabolic reprogramming and mitochondrial biogenesis; FOXO3 acts as the principal oxidative stress sensor with context-dependent neuroprotective or pro-apoptotic outputs; FOXO4 regulates cellular senescence; and FOXO6 maintains synaptic metabolic support. These functions vary across cell types and disease stages, with post-translational modifications determining functional transitions. FOXO proteins participate in complex interactions with disease-specific pathological proteins, either promoting clearance and repair or exacerbating neurodegeneration depending on stress intensity and chronicity. Therapeutic strategies targeting FOXO remain in preclinical and early clinical stages. Key challenges include disease stage-dependent dosing, cell-type-specific delivery, blood-brain barrier penetration, and metabolic side effects. Future directions emphasize biomarker-guided patient stratification and precision interventions aligned with the spatiotemporal dynamics of FOXO signaling. Unlike prior reviews focusing on single pathways or diseases, this work integrates isoform-specific, stage-dependent, and cell-type-resolved FOXO functions into a unifying hierarchical framework. - Source: PubMed
Publication date: 2026/05/21
Lv ZhengxiangLiu XiaodongZhou ZhiweiHuang QinLiu HaijunXu ZucaiXu Ping - Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by the accumulation of amyloid-β, hyperphosphorylation of tau, oxidative stress, synaptic dysfunction, and neuroinflammation. Recent research underscores the Forkhead box O (FOXO) family of transcription factors (FOXO1, FOXO3, FOXO4, FOXO6) as crucial regulators of these pathogenic processes. FOXOs regulate antioxidant defenses, autophagy, mitochondrial quality control, and apoptosis by functioning downstream of insulin/PI3K-Akt and stress-responsive pathways. This context-dependent activity enables FOXOs to act as dual regulators: brief activation improves proteostasis, oxidative stress tolerance, and synaptic resilience, whereas dysregulated signaling triggers pro-apoptotic and neurodegenerative pathways. Genetic and pharmacological studies targeting FOXO signaling highlight its potential as a therapeutic target; nonetheless, obstacles persist, including isoform specificity, compensatory feedback mechanisms, and transport across the blood-brain barrier. This review consolidates contemporary understanding of the structural and functional functions of FOXO isoforms in AD, their participation in amyloid and tau pathology, oxidative stress, and neuroinflammation, and assesses options for therapeutic control. A deeper understanding of FOXO signaling could lead to novel therapies that utilize its neuroprotective properties specifically, while minimizing adverse effects. - Source: PubMed
Publication date: 2026/05/26
Shyam MukulVeronica AleenWadhwa JyotiSharma VidhiB M OveyaaSrirangan PrathapVenkatesh RajendranEvan Prince Sabina