FOXC2 antibody - middle region (ARP32307_T100)
- Known as:
- FOXC2 (anti-) - middle region (ARP32307_T100)
- Catalog number:
- arp32307_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXC2 antibody - middle region (ARP32307_T100)
Related genes to: FOXC2 antibody - middle region (ARP32307_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 - middle region (ARP32307_T100)
Related articles to: FOXC2 antibody - middle region (ARP32307_T100)
- Transcriptional reprogramming has an important role in kidney glomerular disease. Using in vivo murine models of podocyte injury, we studied the roles of the FOXC2 and WT1 transcription factors (TFs) in podocyte injury. Podocytes are a crucial cell type of glomeruli, the filtration units of each nephron. Podocyte injury is often the incipient event leading to chronic kidney disease. It is well established that the TFs FOXC2 and WT1 are required in podocytes to maintain the glomerular filtration barrier. Their role in the response to injury is less well understood. Here, we tested the hypothesis that FOXC2 and WT1 act together to mediate transcriptional reprogramming in response to podocyte injury. Similarly to that of WT1, genome-wide FOXC2 binding to target genes is dynamic during the course of injury, initially increasing, but late in injury there is a dramatic decrease in FOXC2 expression and in its binding to target genes. Podocyte-specific inactivation of FoxC2 or Wt1 in adult mice limits the transcriptional response to injury. Correlating FOXC2 and WT1 ChIP-seq analyses demonstrated that they co-bind many genes expressed in podocytes. Thus, reprogramming the transcriptome involves dynamic changes in the binding of FOXC2 and WT1 to their target genes during a reparative injury response. - Source: PubMed
Publication date: 2026/06/08
Ettou SandrineGreenberg AnyaLee SangyoonRajesh ArjunSun LiangTabibzadeh NahidOishi HarukaKonoe RanMcCown Phillip JEddy SeanDriscoll VictoriaMiyoshi TomoyaHiratsuka KenLam JasonSrinivasan R SathishJung Youngsook LIsaac BijuSun MingweiTaglienti Mary EKeller KeithChen HongKretzler MatthiasWeins AstridMorizane RyujiRockowitz ShiraSchumacher Valerie ALee DongwonKreidberg Jordan A - The omentum is a vascularized, immune-active tissue with regenerative potential, particularly when activated by intraperitoneal stimuli. Its secreted factors may promote lymphangiogenesis, offering a novel approach to lymphedema treatment. - Source: PubMed
Publication date: 2026/05/29
Hojo MasahiroSeo DongkyungIto RiriIshikawa KosukeMiura TakahiroFunayama EmiYamamoto YuheiMaeda Taku - 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