FOXC2 Mouse Monoclonal Antibody
- Known as:
- FOXC2 Mouse Monoclonal Antibody
- Catalog number:
- BIN-002303-M02
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FOXC2 Mouse Monoclonal Antibody
Related genes to: FOXC2 Mouse Monoclonal Antibody
- Gene:
- FOXC2 NIH gene
- Name:
- forkhead box C2
- Previous symbol:
- FKHL14
- Synonyms:
- MFH-1
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-14
- Date modifiied:
- 2019-04-23
Related products to: FOXC2 Mouse Monoclonal Antibody
Related articles to: FOXC2 Mouse Monoclonal Antibody
- 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 - Gelatinous drop-like dystrophy is a rare autosomal recessive disorder caused by pathogenic variants in the gene and characterized by subepithelial amyloid deposits in the cornea. Alterations in are seen in lymphedema-distichiasis syndrome, in which patients classically exhibit lymphedema of the extremities and a double row of eyelashes. This report links alterations in the gene to a corneal phenotype that is histologically identical to that seen in gelatinous drop-like dystrophy. - Source: PubMed
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Sexton GabrielOury Nadine HTripi Kelly SchoopingNischal Ken KChu Charleen T - Peripheral nerve injuries (PNIs) remain a major clinical challenge, often leaving patients with lifelong sensory, motor, and functional impairments despite surgical repair. While gene and cell therapies hold promise, their translation has been hampered by the lack of safe, efficient, and targeted delivery strategies. Here, we introduce vasculogenic tissue nanotransfection (TNT) as a nonviral, reprogramming-based therapeutic platform to enhance nerve regeneration to augment surgical reconstruction. This one-time, millisecond-scale intervention reprograms resident cells in situ toward a vasculogenic phenotype, fostering neovascularization and vascular remodeling to support axonal regeneration. Through integrated in vitro screening and in vivo validation, we identified an optimized formulation of vasculogenic genes (, , and ; ) that maximized reprogramming efficiency and regenerative potential. In a long-segment nerve defect model reconstructed with isografts, TNT-mediated delivery of markedly improved functional recovery, including grip strength and muscle contractility, accompanied by increased vascular density and myelinated axon counts. Together, these findings establish TNT-mediated vasculogenic reprogramming as a transformative adjunct to surgical repair of PNIs, offering a clinically translatable strategy to accelerate nerve regeneration and restore function. - Source: PubMed
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