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
- To explore the correlation between serum fibroblast growth factor 9(FGF9), Sestrin2 and hydroxybutyrate dehydrogenase (HBDH) and the severity of sepsis, and to analyse the predictive value of FGF9, Sestrin2 and HBDH for clinical outcome. - Source: PubMed
He JianLin XinruDing XiangLiu Maoxia - Urolithin A (UA) and urolithin B (UB) are gut microbiota-derived metabolites of ellagitannins reported to influence mitochondrial function, inflammation and muscle metabolism. Their comparative transcriptomic effects in human skeletal muscle cells remain undefined. We characterized UA- and UB-induced molecular responses in primary human myotubes. - Source: PubMed
Henrotin YvesFlorin AntoineSanchez ChristelleCentonze PresciliaCoelho Tiago PintoBekisz SophieDubuc Jean-EmileGaland OlivierLambert Cécile - Hepatocellular carcinoma (HCC) is the predominant histological subtype of primary liver cancer and remains a leading cause of cancer-related mortality because of its molecular heterogeneity, high recurrence rate, and incomplete responses to systemic therapy. Among dysregulated oncogenic networks, fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) signaling contributes to hepatocarcinogenesis, angiogenesis, stromal remodeling, immune escape, and therapeutic resistance. This review critically examines the biological organization and translational implications of FGF/FGFR signaling in HCC, with particular emphasis on the FGF19-KLB-FGFR4 axis and a cautious appraisal of its current translational maturity. FGF2, the FGF8 subfamily, FGF9, and FGF19 drive context-dependent tumor programs shaped by etiology, cirrhosis, stromal interactions, intratumoral heterogeneity, and crosstalk with major oncogenic pathways. Although FGF19-KLB-FGFR4 is the most mature and clinically testable FGF-related therapeutic framework in HCC, selective FGFR4 inhibition is still limited by early-phase clinical evidence, bile-acid-related toxicity, FGFR3/KLB-mediated redundancy, bypass signaling, and acquired resistance. Early clinical data with irpagratinib support the rationale for combining FGFR4 inhibition with immune checkpoint blockade, but definitive validation and reproducible biomarker assays are still needed. Future translation should prioritize prospectively validated biomarker panels, mechanism-based combinations, longitudinal resistance monitoring, and models that recapitulate the cirrhotic, immune-active liver microenvironment. - Source: PubMed
Publication date: 2026/09/17
Jin QiangliLiu YangJin Penghui - A heterozygous Kruppel-like factor 1 (KLF1) E325K mutation causes a severe form of congenital dyserythropoietic anaemia (CDA), designated CDA-IV (Online Mendelian Inheritence in Man, OMIM 613673), a rare disease with only 15 cases known. In addition to haemolytic anaemia, manifest often at birth, four of seven (57%) of 46,XY children with KLF1 E325K mutation exhibit a range of dysmorphic external genitalia including 46,XY complete sex reversal (2/7 or 28.5%). No genital abnormalities were reported in a boy with double heterozygous KLF1 null mutations, suggesting that the KLF1 E325K variant causes, in addition to its negative impacts on erythroid differentiation, disruptions in male sex differentiation. Our studies suggest a role for a cooperative effect of concurrent 'non-pathogenic' polymorphisms in multiple genes associated with disorders of sex differentiation (DSD), notably fibroblast growth factor 9 (FGF9), whose expression was decreased in the gonads and peripheral blood in the case described here. We propose that the combined loss of FGF9 and CD44 (a target for CDA-IV KLF1) resulted FGF9 signalling loss and likely caused 46,XY sex reversal. Our studies also suggest that whole-blood gene expression studies in the proband/parent triad may provide critical clues in evaluating children with DSD, the cause of which remains undiagnosed in many cases. - Source: PubMed
Publication date: 2026/09/17
Ravindranath YaddanapudiCraig Douglas BParajuli PrahladBagla ShrutiSaad AliCukovic DanielaHeikinheimo MarkkuSalonen JonnaRegling KatherineDombkowski AlanDeFalco TonyBieker James J - 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