FOXO1A Mouse Monoclonal Antibody
- Known as:
- FOXO1A Mouse Monoclonal Antibody
- Catalog number:
- BIN-002308-M12
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FOXO1A Mouse Monoclonal Antibody
Related genes to: FOXO1A Mouse Monoclonal Antibody
- Gene:
- FOXO1 NIH gene
- Name:
- forkhead box O1
- Previous symbol:
- FKHR, FOXO1A
- Synonyms:
- FKH1
- Chromosome:
- 13q14.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-07
- Date modifiied:
- 2016-10-05
Related products to: FOXO1A Mouse Monoclonal Antibody
Related articles to: FOXO1A Mouse Monoclonal Antibody
- Recent studies have advanced understanding of chromosomal organization and its role in gene regulation, yet most analyses focus on short-range interactions (<2 Mb), limiting insight into broader architecture. The relationships between topologically associating domains (TADs), sub-TAD loops, cross-TAD interactions, and chromosomal compartmentalization remain poorly understood. Here, using high-resolution Hi-C analysis, we identify extensive multi-megabase and interchromosomal interactions (metaloops) in T lymphocytes that organize into meta-TAD associations (metadomains). These metaloops connect distal promoters and regulatory elements of genes functionally important in T cells, including Ctla4, Ikzf2, Il2ra, Ets1, and Foxo1. Reanalysis of mouse and human datasets confirms their reproducibility and dependence on superenhancers. Genome-wide clustering reveals three distinct interchromosomal hubs, including a superenhancer-enriched hub linked to T cell-specific gene activation. Integrative analysis of regulatory genomics data identifies factors associated with short- versus long-range interactions. This study introduces a broadly applicable computational framework and reveals features of T cell genome organization. - Source: PubMed
Publication date: 2026/05/07
Dolsten GabrielWang Zhong-MinHuang XiaoSong SusieWilson Michael JBing Xin YangKe WenfanCafiero Thomas RNelson Amy NFernando SebastianPloss AlexanderSchedl PaulLevine Michael SViny Aaron DRudensky Alexander YPritykin Yuri - Immune checkpoint inhibitors (ICI), epitomized by PD-1/PD-L1 antibodies, have ushered in a new era in lung cancer treatment. However, ICI monotherapy is only applicable to a small subset of patients with high PD-L1 expression, while most patients with low expression require combination therapies. In this study, we found that β-elemene promotes M1 polarization of tumor-associated macrophages (TAMs) and enhances the efficacy of PD-L1 antibody (aPD-L1) in C57BL/6 mice. RNA sequencing and surface plasmon resonance revealed that β-elemene directly binds to FLT1 and inhibits the PI3K/AKT/FOXO1 signaling pathway, thereby mediating TAMs M1 polarization. Using Flt1 knockout mice, we further validated the critical role of Flt1 in TAMs polarization and confirmed that M1 polarization synergizes with aPD-L1 treatment. Furthermore, co-immunoprecipitation showed that the FLT1 intracellular domain binds to and phosphorylates the p85α subunit, triggering downstream signaling cascades. These findings elucidate the synergistic mechanism between β-elemene and aPD-L1. Moreover, given the clinical availability of both agents, they provide a strong rationale for further clinical evaluation of this combination therapy. - Source: PubMed
Publication date: 2026/05/08
Wang JianminYu YongxinLin FenglinWang HangNian Weiqi - Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory condition with limited treatments. Although macrophages are implicated in its pathogenesis, the mechanisms driving their phenotypic switching remain unclear. This study identifies CCR1's role in IC/BPS and evaluates CCR1 inhibition as a therapeutic strategy. Integrated bulk and single-cell RNA sequencing reveal enrichment of pro-inflammatory CCR1⁺ macrophages in bladder tissue from patients with IC/BPS. In a lipopolysaccharide-induced rat model, pharmacological inhibition of CCR1 suppresses M1 polarization, promotes M2 polarization, and improves pain thresholds, urinary symptoms as well as bladder inflammation. Mechanistically, CCR1 knockdown enhances FOXO1 phosphorylation and degradation, reduces its nuclear translocation, and activates PPARγ signaling to promote M2 polarization. Analysis of clinical samples shows increased CCL7 levels in bladder tissue and urine, with urinary levels correlating with symptom severity. These findings identify CCR1 as a candidate target for further therapeutic evaluation in IC/BPS. - Source: PubMed
Publication date: 2026/05/09
Luo RuixiangLi WenshuangLiu BolongHuang JunlongDing HongluZhang ChiLi XiaoyangWang ZiqiaoLiu ZhengZhou XiangfuChen Jialiang - This study aims to explore the characteristics and differentiation pathways of microglia and macrophages using single-cell transcriptome data from mouse stroke models. The clusters of microglia and macrophages in the middle cerebral artery occlusion model mouse brain were identified using the Seurat package. The signaling pathways were evaluated through Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes analyses, while transcription factor activity was analyzed using DecoupleR. Monocle2 was employed to infer the differentiation trajectory of microglia and macrophages, exploring changes in gene expression patterns during their activation process using gene dynamics analysis. Additionally, the self-differential and overlapping subclusters of macrophages and microglia following cerebral ischemia were assessed, and CellChat was used to analyze differences in cell communication. An oxygen-glucose deprivation model of BV2 microglia was established, and phagocytosis assays and real-time-quantitative PCR were conducted to evaluate the effects of FoxO1 knockdown on the phagocytic ability and inflammatory cytokine production of microglia. Microglia and macrophages showed significant functional changes following ischemic stroke. Microglia enhance their phagocytic capabilities, whereas macrophages exhibited a reduction in phagocytic function. The predominance of microglia in phagocytic and inflammatory pathways is primarily attributed to the differential expression of specific transcription factors, particularly FoxO1. Knockdown of FoxO1 significantly diminished the phagocytic ability of BV2 cells and increased the expression of the inflammatory cytokines CCL2, IFN-γ, and TNF. The transcription factor FoxO1 mediates the functional differences in phagocytosis and inflammatory responses between macrophages and microglia. Activation of FoxO1 can significantly enhance the phagocytic capacity of microglia while simultaneously reducing inflammatory responses, positioning it as a potential new target for the treatment of ischemic stroke. - Source: PubMed
Li DengxingLiao BaoWei HuiminLi FengmeiTeng JinyongWei LiliHuang YueyuanYang QinLi Shaofa - Energy homeostasis relies on interconnected brain circuits that integrate hormonal signals with behavioral outputs. Building upon the established roles of canonical transcriptional regulators like STAT3 and FOXO1 in metabolic neurons, we synthesize emerging evidence positioning basonuclin-2 (BNC2), a deeply conserved zinc-finger transcription factor, as a putative coordinator of energy balance. Spatial transcriptomic mapping highlights selective BNC2 expression within the hypothalamic arcuate nucleus and ventral pallidum. Recent functional studies demonstrate that hypothalamic BNC2 neurons suppress appetite via leptin-driven GABAergic inhibition of AgRP/NPY neurons, whereas ventral pallidum BNC2 neurons modulate reward-driven food intake. Together, these findings suggest BNC2 functions as a critical bridge between homeostatic and hedonic feeding circuits. Future investigations addressing isoform specificity, direct hormonal sensing, and human genetic relevance will be essential to evaluate BNC2 as a therapeutic target for obesity and related metabolic disorders. - Source: PubMed
Publication date: 2026/04/17
Zhang ZixuHu ShengruHua KaiyiLi PengDuan YikeShao WangqiSun ShihaoZhang HongboMu Mingdao