FOXC2 antibody - C-terminal region (ARP31703_T100)
- Known as:
- FOXC2 (anti-) - C-terminal region (ARP31703_T100)
- Catalog number:
- arp31703_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXC2 antibody - C-terminal region (ARP31703_T100)
Related genes to: FOXC2 antibody - C-terminal region (ARP31703_T100)
- 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 antibody - C-terminal region (ARP31703_T100)
Related articles to: FOXC2 antibody - C-terminal region (ARP31703_T100)
- Hematopoietic stem cells (HSCs) rely on specialized niche cells for maintenance, yet how these regulators functionally integrate to preserve hematopoiesis remains unknown. Here, we identified a subset of Procr+ endothelial cells (ECs) with progenitor-like properties in bone marrow (BM), which is critical for vascular homeostasis and injury regeneration. Endothelial-specific ablation of Procr severely compromises BM vascular integrity and function. Beyond serving as a stem cell marker, Procr serves dual biological functions as a functional signaling receptor in multicellular communication. Mechanistically, Procr binds HSPA8 to promote Foxc2 nuclear translocation, upregulating Dll4 transcription to sustain Dll4/Notch3 activation in mesenchymal stem cells (MSCs), revealing a Procr/HSPA8/Foxc2/Dll4 axis essential for EC and MSC crosstalk. Through the HSPA8/Foxc2/Dll4/Notch3 axis, Procr+ ECs instruct MSCs Notch signaling, coordinating their adipogenic-osteogenic differentiation to maintain HSC self-renewal and myeloid output. Building on this mechanism, we demonstrated conserved functionality of Procr+ EPCs in human BM. Human PROCR+ ECs were found to similarly enhance DLL4/Notch3 signaling in MSCs, consequently preserving HSC function, confirming their therapeutic relevance. Our work highlights Procr⁺ EPCs sustain vascular integrity and govern MSC-dependent HSC maintenance, offering targeted clinical strategies for niche regeneration. - Source: PubMed
Publication date: 2026/05/08
Xu ChangLv XueYang ShangdaLv YanlingZheng YaweiWang Yu-XiangHui YanSun GuohuanZhao XiangnanMa Lan-YueDuan HonglinZhang LinminPu ShuangshuangSun LuLi XialinHe YichengFang WenjiaYang MengSuda ToshioChen QiCheng TaoCheng Hui - Despite advances in therapies targeting hemodynamic and neurohormonal axes in heart failure (HF), incomplete reverse remodeling (RR) characterized by persistent myocardial edema and fibrosis remains a major clinical challenge. This review posits that dysfunction of the cardiac lymphatic system, a critical but understudied pathway for interstitial fluid and immune cell clearance, constitutes a fundamental barrier to complete myocardial recovery. We synthesize current evidence outlining the anatomy, developmental biology, and physiological role of cardiac lymphatics in maintaining myocardial fluid homeostasis and immune surveillance. In the context of HF, the lymphatic system undergoes a dynamic evolution: an initial compensatory lymphangiogenic response in the acute phase facilitates the clearance of edema and inflammatory cells, while its subsequent exhaustion or impairment in chronic HF perpetuates a vicious cycle of inflammation, fibrosis, and adverse remodeling. Central molecular pathways, including the VEGF-C/VEGFR-3 axis and transcriptional regulators like PROX1/FOXC2, govern lymphatic growth, integrity, and function. Furthermore, lymphatics actively modulate post-injury immune responses via specialized mechanisms such as CCL21/CCR7-guided cell trafficking. Therapeutically, augmenting cardiac lymphangiogenesis presents a promising strategy to enhance fluid drainage, resolve maladaptive inflammation, and directly support cardiomyocyte survival, thereby creating a conducive milieu for RR. However, translating this potential requires overcoming translational hurdles related to intervention timing, comorbidity-specific lymphatic dysfunction, and the development of targeted delivery systems. This review concludes that harnessing the cardiac lymphatic system represents a paradigm-shifting therapeutic avenue, complementary to existing regimens, with the potential to promote more complete and sustainable reverse remodeling in heart failure. - Source: PubMed
Publication date: 2026/04/22
Huang TingxuanQi TengYao LingjunZhu ZhentaoLi ChenyuTang PengxiangMeng ZeyuWen ZheyuWang TingyuLiu SuiXie PeilinLi ZilinHu Jing - 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
Publication date: 2026/04/11
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
Publication date: 2026/04/08
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