FOXO1A Mouse Monoclonal Antibody
- Known as:
- FOXO1A Mouse Monoclonal Antibody
- Catalog number:
- BIN-002308-M13
- 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
- Muscle atrophy is a major feature of Limb Girdle Muscular Dystrophy R1 (LGMDR1) patients, but its underlying molecular mechanisms have not been fully explored. While the ubiquitin-proteasome system (UPS) is known to be involved in muscle protein degradation, inflammation commonly observed in LGMDR1 patients may further activate the UPS. This study aimed to explore the role of inflammation in the muscle atrophy of LGMDR1 patients. - Source: PubMed
Publication date: 2026/03/30
Banerjee SukanyaRadotra Bishan DassLuthra-Guptasarma ManniGoyal Manoj K - Limited targeted agents are approved for pediatric sarcomas. Tyrosine kinase (TK) inhibitors (TKi) have shown clinical efficacy in some, but not all, young patients with sarcoma. A major obstacle preventing further advances and clinical implementation is the lack of predictive response biomarkers to guide TK-targeted treatments. TK-activating fusions or mutations are rare in these patients. RNA overexpression of TKs is a frequent feature. The unresolved question is when upregulated TK expression is associated with kinase activation and signaling dependence. We explored the TK molecular landscape of 107 patients with sarcoma from the ZERO Childhood Cancer Precision Medicine Program (ZERO) using whole-genome and -transcriptome sequencing. Phosphoproteomic analyses of tyrosine phosphorylation (pY) and functional in vitro and in vivo assays were performed in cell lines and patient-derived xenografts (PDX). Our analysis shows that although novel genomic driver lesions are rare, when present they are therapeutically actionable as exemplified by a novel LSM1-FGFR1 fusion identified in a patient with osteosarcoma. We further show that in certain contexts, TK RNA expression can indicate TK pathway activity and predict TKi sensitivity. We highlight the utility of FGFR inhibitors in PAX3-FOXO1 fusion-positive rhabdomyosarcomas (FP-RMS) characterized by high FGFR4 and FGF8 RNA expression levels and FGFR4 activation (FGFR4_pY). We demonstrate marked tumor growth inhibition in all FP-RMS PDXs treated with single-agent FGF401 (FGFR4-specific inhibitor) and single-agent lenvatinib (multikinase FGFR inhibitor) and report a clinical response to lenvatinib in a patient with relapsed metastatic FP-RMS. Altogether, we identified new patients with sarcoma who may benefit from FGFR inhibitors, most notably FP-RMS via FGFR4/FGF8 coexpression. - Source: PubMed
Publication date: 2026/04/27
Fordham Ashleigh MBrown Lauren MMayoh ChelseaSalib AliceBarger Zara AWong MarieLim Kam Sian Terry C CHu ChangyuanXie JinhanGunther KateTrebilcock PeterTerry Rachael LBarahona PauletteAjuyah PamelaSherstyuk AlexandraAvila AnicaCadiz RoxannePerkins Callum MGifford Andrew JMao JieDolman M Emmy MZhao AndreaO'Regan Luke PGorgels DanielLau Loretta M SZiegler David SHaber MichelleTyrrell VanessaLock Richard BCowley Mark JNicholls WayneDaly Roger JEkert Paul GFleuren Emmy D G - Diabetic kidney disease (DKD) is a major microvascular complication of diabetes Mellitus (DM), characterized by insulin resistance and renal cell apoptosis. Bushen Kai Xuan Tongluo Formula (BKT), a traditional Chinese medicine compound based on the theory of "kidney deficiency, blood stasis, and obstruction of Xuan Fu," shows nephroprotective potential, but its molecular mechanisms remain unclear. This study employed transcriptomic profiling to investigate BKT's renoprotective effects, focusing on the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway in regulating glucolipid metabolism and apoptosis. - Source: PubMed
Publication date: 2026/03/30
Xu MiaoZhao BaoshengWang YouChang YuzhuoLi YujinQin LinglingWang HaiyanJia XiaoleiZheng GuiminLv CuiyanLiu Tonghua - Transcription factor nuclear factor of activated T cells (NFAT) plays a central role in immune gene regulation through cooperative interactions with diverse transcriptional partners. While FOXP family members have been identified as co-regulators of NFAT1, the involvement of other FOX family proteins has remained mechanistically obscure. Here, we solved three crystal structures of NFAT1-RHR/FOXC2-DBD/ARRE DNA ternary complexes and uncovered an unexpected mode of transcriptional repression mediated by FOXC2 through direct, DNA-facilitated binding to the V-shaped groove of NFAT1's Rel-homology region (RHR). Biochemical assays revealed that DNA enhanced FOXC2-NFAT1 interaction by more than five-fold, supporting a model in which DNA acts as a structural co-factor that promotes complex formation. Mutational disruption of the FOXC2-NFAT1 interface impaired complex assembly and abrogated transcriptional repression. Functional assays further confirmed that FOXC2 suppressed NFAT1-driven transcription of multiple cytokines and chemokines, including IL2, TNF, CXCL5, and CCL2. Notably, this repressive mechanism was found to extend to other FOX proteins (FOXI1, FOXO1, and FOXK1), suggesting a broader paradigm of FOX-NFAT1 interaction. Our study defined a previously unrecognized FOX-mediated transcriptional repression mechanism and provides a structural framework for NFAT inhibition by FOX proteins, offering novel insights into the transcriptional regulation of immune-related genes. - Source: PubMed
Chen XiaojuanWu SipengYue SitongZhang LinLiu XueruDai ShuyanLi JunZhang HuajunWei HudieGuo MingQu LingzhiChen LinDeng YalanChen Yongheng - Natural killer cells defend against malignancies and viral infections through a tightly controlled program of differentiation and maturation. However, the transcriptional mechanisms guiding this process remain incompletely defined. Using paired single-cell multiomic profiling, we identify GFI1 as an epigenetic regulator of NK cell differentiation, coordinating EOMES and T-BET transcriptional balance to promote NK cell proliferation and the transition from immature to terminally differentiated NK cell states. GFI1 represses FOXO1 chromatin accessibility in mature NK cells, which normally limits NK cell proliferation and maturation. Co-deletion of both GFI1 and FOXO1 largely rescues NK cell differentiation, identifying a critical GFI1-FOXO1 axis required for protection against tumour metastasis. These findings position GFI1 as a key transcriptional node integrating NK cell differentiation, activation and effector programs. - Source: PubMed
Publication date: 2026/04/22
Huang QiutongChaudhry M ZeeshanDight JamesAlim LouisaYu HuiyangDenman RenaeMan Hiu OnSchreuder JaringGarnham Alexandra LTuong Zewen KSouza-Fonseca-Guimaraes FernandoJacquelot NicolasBelz Gabrielle T