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
- Unravelling causal links between unique structural/copy-number variants (SV/CNV) and associated phenotypes is essential for correct genetic counselling. We investigated two families in which patients with craniosynostosis had SV/CNV potentially dysregulating a fibroblast growth factor (FGF)-encoding gene; a 730 kb dup(4)(q21.21) including FGF5; and a complex 568 kb interspersed 13q12.11 duplication, located 841 kb from FGF9. - Source: PubMed
Publication date: 2026/09/08
Korona DagmaraHashimoto Akiko SonedaPei YangCalpena EduardoSloane-Stanley JackieRiva Simone GSchwessinger RonForzano FrancescaChintawar SatyanDuggal GalbhaWall Steven AHughes Jim RTwigg Stephen R FWilkie Andrew O M - Fatty liver hemorrhagic syndrome (FLHS) is a metabolic disease of laying hens that reduces egg production and is accompanied by reproductive impairment, but the ovarian regulatory mechanisms that connect nutritional stress to follicular dysfunction remain unclear. This study examined whether active chromatin remodeling in the ovary is associated with FLHS induced by a high-energy, low-protein (HELP) diet. Hy-Line Brown hens were assigned to a basal diet or HELP diet, and ovarian tissue was collected for histone H3 lysine 27 acetylation (H3K27ac) chromatin immunoprecipitation sequencing and RNA sequencing. The HELP diet reduced laying performance and the numbers of small yellow and hierarchical follicles, indicating compromised follicular development. Genome-wide H3K27ac profiling identified 2,111 regions with lower acetylation and 1,707 regions with higher acetylation in FLHS ovaries. Genes linked to differential H3K27ac regions were enriched in pathways related to oocyte meiosis, cell cycle control, FoxO signaling, gonadotropin-releasing hormone signaling, and steroid hormone biosynthesis. RNA sequencing identified 341 differentially expressed genes, with a predominance of downregulated genes. Integration of chromatin and transcriptome data highlighted folliculogenesis-related genes, including FGF1, FGF9, and MMP10, that showed reduced H3K27ac enrichment together with decreased expression. Super-enhancer analysis further identified 131 regions with reduced H3K27ac signal in FLHS ovaries, including regions located near PCNA and RAP1A, two genes involved in cellular proliferation and survival signaling. Motif enrichment of differential H3K27ac regions implicated Fos, SF-1/NR5A1, and GATA-4 as candidate transcriptional regulators. These findings indicate that HELP diet-induced FLHS is associated with broad attenuation of active ovarian regulatory elements and reduced expression of genes required for follicle growth, tissue remodeling, and steroidogenic function. The study provides an ovarian epigenomic framework for understanding reproductive decline in FLHS-affected laying hens. - Source: PubMed
Publication date: 2026/07/05
Cui YongZeng WenhuiLiang HaipingWang YujieWeng LinjianQu MingWei QingXie XianhuaHuang Jianzhen - - Source: PubMed
- Age-related cataract (ARC) is the most prevalent form of cataract. Oxidative stress-induced apoptosis of lens epithelial cells (LECs) is a major pathogenic factor, but its underlying molecular mechanisms remain incompletely understood. This study investigated the roles of FGF9, ERK, and MMP9 in ARC and examined whether the FGF9/ERK/MMP9 pathway is involved in the protective effects of (-)-epigallocatechin-3-gallate (EGCG) against LEC apoptosis. FGF9 and MMP9 were downregulated at both the mRNA and protein levels in ARC mice and HO (200 µM)-treated HLE-B3 cells as determined by immunohistochemistry, Western blotting and qRT-PCR. FGF9 overexpression increased cell viability and reduced apoptosis in HO-treated HLE-B3 cells, as demonstrated by CCK-8 and Hoechst 33342 staining. EGCG treatment improved cell viability and increased FGF9 expression in HO-treated cells and lens tissues from ARC mice. Conversely, FGF9 knockdown attenuated the protective effect of EGCG. Further experiments suggested that FGF9 may contribute to the anti-apoptotic effects of EGCG by modulating ERK phosphorylation and MMP9 expression. ERK activation by TBHQ increased the viability of HO-treated HLE-B3 cells, whereas ERK inhibition with PD98059 attenuated the protective effects of EGCG and decreased MMP9 expression. Moreover, MMP9 knockdown increased cleaved caspase-9 expression and was accompanied by increased apoptosis in LECs. These findings suggest that the FGF9/ERK/MMP9 pathway is involved in oxidative stress-induced LEC apoptosis and may contribute, at least in part, to the protective effects of EGCG in experimental models of ARC. - Source: PubMed
Yu JialeWu YifanWu JiananShi CuigeChen XiaofengWei YingGuan LinaHe JialingZhang YueXiang ZihanSu DongmeiHu ShanshanMa Xu - Baricitinib, a selective JAK1/JAK2 inhibitor with established anti-inflammatory properties, has demonstrated therapeutic efficacy in several autoimmune and inflammatory diseases. This study aimed to investigate the neuroprotective potential of baricitinib in a ketamine-induced rat model of schizophrenia. Specifically, the study examined its effects on behavioral deficits, neurochemical alterations, and neuroinflammatory responses, while exploring the association of the JAK2/STAT3 and PI3K/AKT/mTOR signaling pathways with its neuroprotective effects. Schizophrenia-like symptoms were induced by intraperitoneal administration of ketamine (30 mg/kg) for five consecutive days, followed by oral treatment with baricitinib (5 or 20 mg/kg/day) for 14 days. Ketamine administration produced significant locomotor hyperactivity, social withdrawal, and cognitive impairment, accompanied by reduced dopamine D2 receptor (D2R), contrary to elevating fibroblast growth factor 9 (FGF9), NLRP3 expression, and pro-inflammatory cytokines including interleukin-1β, interleukin-6, and tumor necrosis factor-α in both the hippocampus and prefrontal cortex. These changes were associated with marked hyperactivation of the JAK2/STAT3 and PI3K/AKT/mTOR pathways. Treatment with baricitinib, particularly at the higher dose (20 mg/kg), significantly attenuated behavioral deficits, restored D2R expression, suppressed FGF9 and NLRP3 levels, reduced pro-inflammatory cytokine production, and normalized aberrant signaling pathway activation. Histological analysis further confirmed preservation of neuronal integrity in both brain regions. These findings indicate that baricitinib exerts robust neuroprotective effects in a ketamine model of schizophrenia, accompanied by attenuation of neuroinflammation and modulation of the JAK/STAT and PI3K/AKT/mTOR pathways. The present results suggest that baricitinib may represent a promising therapeutic candidate for mitigating neuroimmune dysregulation associated with schizophrenia-like alterations. - Source: PubMed
Publication date: 2026/08/19
Albariqi Ali ANawwar Dalia AIbrahim Weam WKhattab Mahmoud M