FGF20 Antibody (C-term)
- Known as:
- FGF20 Antibody (C-terminus)
- Catalog number:
- AP19307b
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- FGF20 Antibody (C-term)
Related genes to: FGF20 Antibody (C-term)
- Gene:
- FGF20 NIH gene
- Name:
- fibroblast growth factor 20
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-19
- Date modifiied:
- 2015-09-07
Related products to: FGF20 Antibody (C-term)
Related articles to: FGF20 Antibody (C-term)
- Environmental toxicants (ENVOTOX) have emerged as critical risk factors for congenital malformations (CMFs) in the modern industrial era. Although epidemiological evidence underscores their adverse impact on pregnancy outcomes, the underlying molecular mechanisms remain insufficiently defined. This review consolidates current insights into exposome toxicity profiling, developmental pathway disruptions, and molecular mapping to identify potential biomarkers and mechanistic links between ENVOTOX and CMFs. Protein-protein interaction (PPI) network analysis identified 35 CMF-associated proteins, with ten fibroblast growth factors (FGFs: FGF4, FGF5, FGF8, FGF9, FGF10, FGF16, FGF17, FGF18, FGF20, and FGF22) prioritized as hub nodes. Molecular docking analysis showed high binding affinity of FGF9 and FGF4 toward dioxin-associated toxicants, with dibenzo-p-dioxin (DBPDO) exhibiting the strongest interaction (binding energy: -7.2 kcal/mol), followed by polychlorinated dibenzofurans (PCDBFs) (-6.7 kcal/mol) with FGF9. Notably, FGF9 exhibited mutagenic binding potential at ASN146, mediated through π-donor hydrogen bonding with DBPDO. Comparative toxicity data further highlighted the acute risks, as DBPDO demonstrated a lower LD (2.26 mol/kg) relative to PCDBFs (4.134 mol/kg). Collectively, this review emphasizes the central role of FGFs in mediating ENVOTOX-induced teratogenicity and offers molecular-level perspectives to guide biomarker discovery and intervention strategies for mitigating CMF risk. - Source: PubMed
Shukla Adarsh KumarMahajan RashmiTyagi Anuj KumarSwaroop Kamendra - Schwann cell mitochondrial damage plays an important role in diabetic neuropathic pain (DNP). Fibroblast growth factor 20 (FGF20) has been shown to protect nerve cells and regulate neural function, but its function and mechanism in DNP remain unclear. - Source: PubMed
Publication date: 2026/07/14
Ning YaLiang YueweiHuang Youqing - Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are pathologically characterized by disruption of the alveolar-capillary barrier, excessive inflammatory responses, and dysregulated intra-pulmonary coagulation. Although inflammatory and thrombotic cascades have been extensively studied, endogenous epithelial-derived signaling mechanisms coordinating barrier stabilization with immunothrombotic restraint remain undefined. Here, we identify fibroblast growth factor 20 (FGF20) as a constitutive epithelial regulator suppressed in alveolar barrier-associated cells during sepsis-induced ALI. In a CLP rat model, both prophylactic and therapeutic administration of recombinant human FGF20 (rhFGF20) improved 7-day survival, attenuated pulmonary edema and inflammation, restored gas exchange, and preserved alveolar-capillary integrity. rhFGF20 restrained procoagulant and antifibrinolytic mediators tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) while suppressing NF-κB activation. Mechanistically, FGF20 acted through fibroblast growth factor receptor 1 (FGFR1) to engage the FGFR1-PI3K-AKT cascade. AKT activation bifurcated into two axes: (i) inhibition of NF-κB phosphorylation and nuclear translocation, restraining TF/PAI-1 transcription; and (ii) inhibitory phosphorylation of glycogen synthase kinase 3β (GSK3β) at Ser9, stabilizing epithelial and endothelial junctional proteins (E-cadherin, VE-cadherin, ZO-1). Pharmacological inhibition of FGFR1 or AKT abolished both barrier-protective and anticoagulant effects, confirming pathway dependency. Clinically, serum and bronchoalveolar lavage fluid FGF20 levels were reduced in ARDS patients and positively correlated with PaO₂/FiO₂ ratios, linking reduced FGF20 to disease severity. Collectively, these findings position FGF20 as an upstream integrator of structural and immunothrombotic homeostasis within the alveolar-capillary unit. Restoration of the FGF20-FGFR1 axis reconstitutes a proximal checkpoint stabilizing barrier architecture and constraining NF-κB-dependent procoagulant activation, highlighting FGF20 as a mechanistically grounded therapeutic target in sepsis-induced ALI/ARDS. CLINICAL SIGNIFICANCE. - Source: PubMed
Publication date: 2026/05/05
Dong QiTao JunlingYuan JiaTian JunyuanCheng YumeiWang JingniXiao ChuanChen XianjunWang YingLi WeiShen Feng - Hemodialysis (HD) patients suffer from chronic inflammation which is a serious complication and contributes significantly to morbidity and mortality. Dialysis technology has advanced over many years but despite advances, its underlying molecular mechanism remains poorly understood. We have designed an exploratory study and investigated how hemodialysis influences epigenetic changes by understanding the DNA methylation patterns which are associated with inflammation. By using the same polysulfone (PS) membrane dialyzer, we have collected the blood samples from the patients before and after dialysis. For DNA methylation analysis, we have extracted genomic DNA using the Monarch® Genomic DNA Purification Kit. Bisulfite conversion was done using the QIAGEN Epitect Bisulfite Kit. Genome Studio, which is a computational software, was used to identify the DNA methylation profiles. These profiles revealed significant epigenetic changes across the hemodialysis patients’ samples. From these DNA methylation profiles, we identified the differential methylated regions (DMRs) and focused on the genes that are associated with these DMRs with the change greater than 80% to confirm robustness. We identified the chromosomal mapping of DMR-associated genes on CpG islands and shore localization, promotor or enhancer regions, to evaluate the functional impact of methylation changes. One of the bioinformatics tools, named Discovery Annotation, Visualization, Integration Database (DAVID) was used to perform functional enrichment analysis to identify the affected biological pathways involved in neuronal signaling, immune regulation, inflammation, and metabolism. Protein- Protein Interaction network was constructed using another bioinformatics tool, named String Database, and It analysis was performed using a bioinformatics desktop-based tool called Cytoscape, which helped in identifying critical hub genes including TWIST1, SHANK3, FGF20, MEF2C, RUNX2, CAV1, CDKN2A, WNT3A, and CXCL12, which play crucial roles in immune system compromise and inflammatory regulation. A total of 93 genes, across the samples of HD patients, showed significant methylation alterations. Of which, 41 genes showed changes exceeding 100% and mostly mapped on Promoter/enhancer regions at CpG islands and shores. In HD patients, these functional consequences suggest changes in their role in impaired vascular function, cognitive decline and immune dysregulation. Fibrinogen (FB) behaviour during dialysis, particularly its adsorption onto the dialysis membranes, was understood using Synchrotron Imaging at the Canadian Light Source (CLS) which provided us a high-resolution visualization. To confirm significant FB fouling between initial and intermediate membrane layers, these targeted regions were identified using raw CT scan images and their magnified views. Similarly, we identified that the level of inflammatory biomarkers, which were elevated in post-dialysis samples of HD patients including vWF, CRP, Serpin C1, Properdin, and PF4 indicating an amplified inflammatory response. Particularly, the critical hub genes that are associated with vascular regulation including CAV1, TWIST1, CDKN2A, and CXCL1, were reported as hypermethylated after dialysis, meaning their expression may reduce which affects their contribution in endothelial dysfunction. These findings suggest a self-perpetuating inflammatory loop, where FB adsorption initiates molecular and immunological responses that reinforce epigenetic dysregulation. One of the important limiting factors is sample size, which influenced the reliability of findings across the molecular and clinical levels, and this underlines that further investigation is needed. This study helped us designed the foundational insights to target the anti-inflammatory strategies that may lead us to the development of more hemocompatible dialysis membranes to reduce long-term complications in HD patients. - Source: PubMed
Publication date: 2026/04/27
Syeda HiraBahig JumanahShoker AhmedSakharkar Meena KishoreAbdelrasoul Amira - Microglia play dual roles in neuroinflammation, driving either detrimental M1 or protective M2 polarization, which critically impacts the outcomes of ischemic stroke. While fibroblast growth factor 20 (FGF20) is established as a neurotrophic factor with neuroprotective properties, its role in regulating microglial polarization remains unclear. This study investigated a novel function of FGF20 in alleviating post-stroke neuroinflammation and its underlying mechanisms. In a rat model of middle cerebral artery occlusion (MCAO), intracerebroventricular administration of FGF20 significantly reduced infarct volume and improved neurological function. RT-PCR analysis revealed that FGF20 bidirectionally regulated cytokine expression, suppressing M1-associated markers (CD86, IL-1β, IL-6, iNOS, TNF-α) while enhancing M2-associated markers (IL-10, Arg-1). Immunofluorescence staining demonstrated that FGF20 attenuated microglia activation in peri-infarct striatum and hippocampus. In vitro, FGF20 counteracted LPS-induced M1 polarization in primary microglia, downregulated the TLR4/NF-κB pathway, and upregulated TREM2 expression. Notably, while the selective FGFR1 inhibitor PD173074 abolished FGF20-induced TREM2 upregulation, it did not reverse the suppression of TLR4/NF-κB, indicating that these two effects are mediated through distinct regulatory mechanisms. These phenotypic shifts were further confirmed by a reduction in CD32/16 (M1) cells and an increase in Arg1 (M2) cells. Mechanistically, FGF20 restored the balance between TREM2 and TLR4 signaling, inhibiting NF-κB activation and attenuating neuroinflammatory responses. Collectively, our findings identify FGF20 as a novel dual modulator of microglial polarization that integrates TREM2-mediated immunoregulation with FGFR1-dependent and independent suppression of TLR4/NF-κB pathway. Thus, FGF20 represents a promising therapeutic candidate for ischemic stroke, extending its functional profile from neuroprotection to targeted immunomodulation through phenotype-specific regulation of microglial polarization. - Source: PubMed
Publication date: 2026/03/08
Zhu LiyunGuo ShufeiWang ZhengyiHuang MinLiu MengfanRuan LixinZou YuchiLin LiWang Xue