Ask about this productRelated genes to: FZD4 antibody
- Gene:
- FZD4 NIH gene
- Name:
- frizzled class receptor 4
- Previous symbol:
- EVR1
- Synonyms:
- CD344
- Chromosome:
- 11q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2016-01-15
Related products to: FZD4 antibody
Related articles to: FZD4 antibody
- Our meta-analysis of 99 studies (463 patients) clarifies key controversies in familial exudative vitreoretinopathy. We found that nearly half of patients are asymptomatic at diagnosis, underscoring the need for early screening in at-risk individuals. Pathogenic mutations (most commonly in FZD4, LRP5, NDP) were identified in 43% of cases. Critically, treatment analysis suggests that combination therapy (laser + anti-vascular endothelial growth factor) was associated with a reduced incidence of retinal detachment in early-stage disease, and vitrectomy was associated with improved anatomical outcomes in advanced stages. These findings provide evidence for genotype-aware, stage-based management. - Source: PubMed
Publication date: 2026/05/05
Tao Le-RanZhang Wen-FeiChen Ya-NingWang Zi-ChengZhao Xin-YuLiu Sheng-Zhi - Human nephrogenesis is complete at 34-36 weeks gestation, with 60% of nephrons forming during the third trimester through lateral branch nephrogenesis (LBN). Currently, no mechanism exists for LBN as there are no late gestation human kidney transcriptional datasets. We hypothesized that an induced but dividing population of nephron progenitor cells (NPCs) would contribute to the amplification of nephrons in late gestation. We used the rhesus macaque, an established model of LBN, to help identify potential mechanisms. - Source: PubMed
Publication date: 2026/05/04
Thakkar KairaveeYarlagadda SunithaAlkhudairy LyanPotter AndrewThorner KonradChaturvedi PraneetCebrian CristinaMcCracken Kyle WSalomonis NathanKopan RaphaelSchuh Meredith P - Inducing transplant tolerance to achieve long-term graft survival without immunosuppression remains a central objective in liver transplantation. - Source: PubMed
Publication date: 2026/04/17
Zhou LinZhao YangWang JingChen QingJia Ya-NanPan Li-ChaoWang Han-XuanYang Hong-WeiHe QiangLi Xian-LiangLang RenDu Guo-Sheng - Blood-brain barrier (BBB) disruption is a key pathological event following traumatic brain injury (TBI), yet its molecular and spatial characteristics remain incompletely understood. Here, we developed a dual dye-labeling system to assess the temporal and spatial dynamics of BBB permeability following controlled cortical impact (CCI) injury in (KO) and (WT) mice. By tracking Evans Blue Dye (EBD), sodium fluorescein (NaFl), and IgG deposition, we reveal distinct patterns of extravasation in the injured cortex and hippocampus. NaFl, a small-molecule tracer, continues to extravasate for 7 days post-injury, whereas EBD leakage diminishes after 4 days. Notably, EC-specific EphA4 KO mice exhibit a protective role in BBB integrity. To further investigate BBB regulation, we integrated spatial transcriptomics with dye quantification, revealing that EphA4 EC ablation upregulates key BBB-related genes () and neuroprotective genes ( and ). Notably, Wnt signaling genes are upregulated in the KO cortex, and we demonstrate that inhibition of Frizzled-4 (FZD4)/Wnt attenuates BBB protection in KO mice. Importantly, direct pharmacological activation of Wnt signaling with the FZD4 agonist FZM1.8 reduces lesion volume and BBB disruption. Overall, these findings demonstrate the effectiveness of spatial transcriptomics and dual-dye labeling in uncovering region-specific transcriptional changes associated with BBB disruption following CCI injury and in assessing the influence of EphA4/Wnt signaling. Wnt signaling emerges as a promising pathway for BBB protection and repair following TBI, offering a potential strategy to mitigate secondary brain injury. - Source: PubMed
Publication date: 2026/04/09
de Jager CarolineJu JingCorbo MarcoPatel KaranTheus Michelle - As the most common microvascular complication of diabetes, diabetic retinopathy (DR) has become a leading cause of blindness among the global diabetic population. The pathogenesis of DR is not yet fully understood, and current clinical treatment options are limited and have suboptimal efficacy. A detailed investigation of the intercellular communication mechanisms during the progression of DR is of paramount importance. In this study, we first synthesized findings from various studies on classical pathways, including VEGF signaling, oxidative stress, inflammatory cascades, the polyol pathway, PKC signaling, and the Wnt/β-catenin pathway, with a focus on elucidating the cell-type specificity of each pathway and the interactions among them. Subsequently, we explored emerging mechanisms identified in recent years, such as the ethanolamine pathway, ANGPTL4, Lrg1, and Norrin-FZD4, to expand our understanding of the pathogenesis of DR. Through a systematic investigation of multiple pathways, we propose that the progression of DR is not driven by the effect of a single pathway but rather results from the dynamic interplay among these signaling networks. Additionally, we described recent advances in the clinical translation of related pathways, including multitarget therapeutic strategies and precision interventions mediated by pathway-specific biomarkers. This review aims to provide a comprehensive and integrative perspective on the mechanisms underlying DR, thereby establishing a theoretical foundation for experimental research and clinical translation. - Source: PubMed
Publication date: 2026/04/13
Wu ShenhaoGao Jing