Human Fibroblast Growth Factor 9 ELISA , FGF9
- Known as:
- Human Fibroblast Growth Factor 9 Enzyme-linked immunosorbent assay test , FGF9
- Catalog number:
- E01F0073
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Fibroblast Growth Factor 9 ELISA FGF9
Related genes to: Human Fibroblast Growth Factor 9 ELISA , FGF9
- Gene:
- FGF9 NIH gene
- Name:
- fibroblast growth factor 9
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 13q12.11
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-15
- Date modifiied:
- 2016-10-05
Related products to: Human Fibroblast Growth Factor 9 ELISA , FGF9
Related articles to: Human Fibroblast Growth Factor 9 ELISA , FGF9
- Osteoarthritis (OA), a prevalent age-related joint disease affecting over 250 million people globally, currently lacks effective disease-modifying treatments. Fibroblast growth factor 9 (FGF9) has shown cartilage-protective effects in post-traumatic OA models, but its role in chondrocyte degeneration and OA pathogenesis remains unclear. This study investigates FGF9's function in human and murine chondrocytes and its therapeutic potential for OA. - Source: PubMed
Publication date: 2026/06/03
Lo Yuan-ShunChen Tsung-MingHuang Teng-LeLiu Yu-ChiaChang Chu-HanChen Chia-YangHsieh Hung-LunTsai Chun-HaoYeow Yi-XueWang Chia-JouChen Ya-Huey - The aim of this study was to compare serum levels of Fibroblast Growth Factor-2 (FGF-2) and Fibroblast Growth Factor-9 (FGF-9) between patients with Bipolar Disorder (BD) and healthy controls (HC), and to evaluate whether these molecules could serve as potential biomarkers for mood episodes (manic/depressive). - Source: PubMed
Publication date: 2026/05/26
Keskin BetülErdoğan AliKüçükçetin İkbal ÖzenCinemre BuketMetin ÖzmenKarabulut SercanAkbaş Sadıka HalideKulaksızoğlu BurakGülkesen Kemal Hakan - The fat mass and obesity-associated gene () has been shown to play a critical role in fat deposition in both humans and livestock. However, its involvement in subcutaneous and intramuscular fat deposition in chickens remains underexplored. In this study, we investigated the regulatory effects and pathways of on subcutaneous and intramuscular fat deposition in chickens through functional gene verification and bioinformatics analysis. Our results demonstrated that, compared to the control group, exogenous transfection of an lentiviral overexpression vector significantly inhibited cell proliferation and increased lipid accumulation in both subcutaneous and intramuscular adipocytes ( < 0.05). Furthermore, transfection of siRNA markedly increased cell proliferation and reduced lipid accumulation in both subcutaneous and intramuscular adipocytes. A total of 413 and 164 differentially expressed genes were regulated by in subcutaneous and intramuscular adipocytes, respectively. Pathway analysis revealed that the regulation of the actin cytoskeleton was a key process involved in -mediated fat deposition in both subcutaneous and intramuscular adipocytes. Additionally, and (subcutaneous fat), as well as , , , and (intramuscular fat), were identified as key genes enriched in this pathway. In conclusion, differentially regulates fat deposition in chicken subcutaneous and intramuscular adipocytes by targeting distinct functional genes within the actin cytoskeleton pathway. - Source: PubMed
Publication date: 2026/05/14
Huang Hua-YunKong YiLi Chun-MiaoSui Yu-LeWang Qian-BaoZhao Zhen-HuaKong Ling-LinWu Zhao-LinHan Wei - DICER1 syndrome is a complex autosomal dominant tumor predisposition disorder characterized by a distinct chronological progression of benign and malignant lesions. By mapping the transition from early-childhood pulmonary and renal manifestations to the adolescent emergence of endocrine and reproductive neoplasms, this review provides a longitudinal framework for clinical vigilance. Central to this analysis is the molecular "two-hit" mechanism, specifically investigating how somatic hotspot mutations in the RNase IIIb domain disrupt the miR-140/FGF9 signaling axis and the feedback loop. The review identifies the neomorphic "Argonaute strand switch" as a primary driver of pathogenesis, resulting in a diagnostic 3p-strand bias that fuels sarcomatous transformation. Beyond the molecular substrate, we define the critical radiographic and clinical markers of malignancy, such as rapid volumetric growth, cystic solidification, and the detection of somatic hotspots via high-sensitivity droplet digital PCR. By integrating the 2024 international surveillance standards with emerging technologies, including Vision Transformer-based radiographic analysis and circulating tumor DNA monitoring, this review offers a proactive, evidence-based roadmap for identifying the predictors of malignancy and better management of the disease. Ultimately, this synthesis aims to equip clinicians and other healthcare profesionals with the predictive tools necessary to achieve definitive cures while minimizing the cumulative clinical and psychological burden on this genetically vulnerable population. - Source: PubMed
Publication date: 2026/04/03
Karthikeyan VarshaAgrawal Devendra K - Fibroblast growth factor (FGF) signaling plays an important role in the pathogenesis of various respiratory diseases, including idiopathic pulmonary fibrosis (IPF). FGF ligands can exert both pro- and anti-fibrotic effects, depending on the responding cell, the expression levels of FGF receptors (FGFR1-4) and the context of other signaling molecules such as Transforming growth factor β (TGF-β). We evaluated here the effect of a modified version of a soluble FGFR3 decoy receptor (designated as "sFGFR3-Fc"), that specifically sequesters pro-fibrotic FGFR3 ligands, FGF1, FGF2 and FGF9 as a potential anti-fibrotic drug. We showed that FGF2 stimulated proliferation and expression of various fibrotic markers in human pulmonary fibroblasts from healthy donors and IPF patients. The sFGFR3-Fc was able to reduce these FGF2-mediated responses and also partially attenuate the pro-fibrotic phenotype induced by TGF-β, including gel contraction. Furthermore, single cell transcriptomic analyses revealed heterogeneity of IPF-derived fibroblasts for FGF2 response and confirmed the potential efficacy of sFGFR3-Fc in decreasing the expression of a subset of TGF-β1 pathway genes. Finally, sFGFR3-Fc was shown to improve the progression of pulmonary fibrosis using both a preventive and therapeutic strategy, evaluated in the standard single bleomycin (BLM) instillation mouse model as well as in a more severe model of repeated BLM instillations, as evidenced by the reduction in ECM deposits, the recovery of body weight and the restoration of lung function. Our data highlight the interplay between the TGF-β and the FGF signaling pathways and demonstrate the potential of targeting pro-fibrotic FGFR3 ligands as therapeutic strategy for IPF. - Source: PubMed
Publication date: 2026/02/21
Scribe CéliaGonçalves DiogoGautier-Isola MarineDellugat PierreRignol GuylèneGhilain ClaireMarsault RaphaelEtasse LauraTruchi MarinCadis HugoMille JessicaGuardini LaetitiaVassaux GeorgesDelgado Cohen JustinPizarro Javier GCheng Seng HCzech ChristianMari BernardHerbert Corentin