Fibroblast growth factor 19 FGF19
- Known as:
- Fibroblast growth factor 19 FGF19
- Catalog number:
- CG74
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Fibroblast growth factor 19 FGF19
Related genes to: Fibroblast growth factor 19 FGF19
- Gene:
- FGF19 NIH gene
- Name:
- fibroblast growth factor 19
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2016-10-05
Related products to: Fibroblast growth factor 19 FGF19
"Recombinant Mouse epidermal growth factor_EGF""Recombinant Mouse epidermal growth factor_EGF""Recombinant Mouse epidermal growth factor_EGF""Recombinant Mouse epidermal growth factor_EGF""Recombinant Mouse Vascular endothelial growth factor D_VEGFD ""Recombinant Mouse Vascular endothelial growth factor D_VEGFD ""Recombinant Mouse Vascular endothelial growth factor D_VEGFD ""Recombinant Mouse Vascular endothelial growth factor D_VEGFD "α-Mating Factor Pheromone, yeastα-Mating Factor Pheromone, yeast(-)-Indolactam V-combined with growth factors, can direct the differentiation of hESCs to Pdx1-expressing pancreatic progenitors(-)-Indolactam V-combined with growth factors, can direct the differentiation of hESCs to Pdx1-expressing pancreatic progenitors(Ala1)-PAR-4 (1-6) (mouse)
(Ala1)-Thrombin Receptor-Like 3 (1-6) (mouse), (Ala1)-Proteinase Activated Receptor 4 (1-6) (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) (mouse), AYPGKF 98%(Ala1)-PAR-4 (1-6) amide (mouse)
AYPGKFamide, (Ala1)-Thrombin Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Proteinase Activated Recepto(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II Related articles to: Fibroblast growth factor 19 FGF19
- Traditional risk factors do not fully account for the residual cardiometabolic risk of major adverse cardiovascular events (MACE) in coronary artery disease (CAD). We aimed to identify circulating metabolic signatures associated with MACE susceptibility and uncover potential pathobiological mechanisms underlying the gut-liver-heart axis. - Source: PubMed
Publication date: 2026/08/12
Lin Min-QingWong Chun-KaAu Ka-WingCheung Chloe Yu-YanLau Yee-ManLiao Song-YanLam Karen Siu-LingXu AiminTse Hung-Fat - This study aimed to explore the association of long-term left ventricular assist device (LVAD) support with changes in inflammation and cardiac remodelling in subjects with advanced heart failure (HF). - Source: PubMed
Publication date: 2026/08/11
Hlavacek DanielCinkajzlova AnnaKollar MarekKasperova Barbora JuditaMelenovsky VojtechMraz MilosHaluzik MartinIvak PeterStemberkova Hubackova Sona - Endocrine fibroblast growth factors (FGF19 subfamily) play a key role in regulating metabolic homeostasis in vertebrates. However, their functional diversification in salmonids remains poorly understood. In this study, we conducted an integrative characterisation of Fgf19 and Fgf21 signalling in rainbow trout (Oncorhynchus mykiss) by combining phylogenetic, structural and expression analyses. Phylogenetic analyses revealed the conservation of single fgf19 and fgf21 genes, despite the extensive expansion of receptors post-Ss4R (salmonid-specific fourth-round whole genome duplication). Structural modelling and molecular dynamics simulations demonstrated the stable interactions of both ligands to multiple Fgfr isoforms, with receptor-specific energetic profiles and conserved core interaction residues. Tissue expression profiling revealed clear differences from mammalian models, such as predominant hepatic fgf19 expression and the absence of hepatic fgf21 under basal conditions. In addition, there were complex and tissue-dependent distributions of fgfr and klotho transcripts. These findings support a receptor-driven diversification model of endocrine Fgf signalling in salmonids, suggesting enhanced endocrine plasticity associated with the retention of receptors following post-genomic duplication. Taken together, our findings provide new insights into the structural and regulatory organisation of endocrine Fgf signalling, as well as its potential role in metabolic regulation in rainbow trout. - Source: PubMed
Publication date: 2026/08/06
Calo JessicaFerreiro DavidPérez-Tierra GabrielSoengas José LuisVelasco Cristina - Cholestatic liver fibrosis is a progressive liver disease characterized by disrupted bile acid homeostasis, persistent inflammation, and excessive extracellular matrix deposition, for which effective pharmacological therapies remain limited. Although Notoginsenoside R1 (NG-R1), a major bioactive saponin from Panax notoginseng, exhibits anti-fibrotic activity in experimental liver injury, its disease-specific mechanism in cholestatic liver fibrosis remains unclear. Here, C57BL/6 mice subjected to bile duct ligation (BDL) were treated with NG-R1 for 14 days. NG-R1 significantly improved liver function, alleviated hepatic and intestinal injury, suppressed inflammatory responses, and attenuated liver fibrosis. Mechanistically, NG-R1 restored intestinal FXR-FGF15 endocrine signaling by enhancing ileal FXR expression and increasing circulating FGF15 levels, thereby contributing to improved gut-liver bile acid homeostasis. Consistent with these changes, hepatic CYP7A1 expression was reduced, bile acid transporters were coordinately regulated (upregulation of BSEP and OSTα/β and downregulation of NTCP), and hepatic bile acid accumulation was decreased. In Caco-2 cells, NG-R1 increased the expression of FXR, FGF19, Occludin, and ZO-1, whereas these effects were partially abolished by the FXR antagonist guggulsterone, supporting direct activation of intestinal FXR signaling. NG-R1 also partially corrected BDL-induced gut microbial dysbiosis. Collectively, these findings suggest that modulation of the intestinal FXR-FGF15 endocrine axis and restoration of gut-liver bile acid homeostasis contribute to the protective effects of NG-R1 against cholestatic liver fibrosis, providing a mechanistic basis for its therapeutic potential. - Source: PubMed
Publication date: 2026/08/05
Yang MinMa QiaolianYang BairongLi JieChang WeiyuCui XiumingNiu BenGe Feng - ObjectivePrevious studies have suggested potential associations between cathepsins and cholelithiasis. This study aimed to investigate the potential causal relationships among cathepsins, inflammatory proteins, and cholelithiasis using Mendelian randomization (MR), and to explore whether inflammatory proteins mediate the association between cathepsins and cholelithiasis.MethodsWe conducted a two-sample MR study using genome-wide association study (GWAS) summary statistics for cathepsins, inflammatory proteins, and cholelithiasis. Genetic associations for cathepsins were obtained from the INTERVAL study of European-ancestry individuals. GWAS data for inflammatory proteins and cholelithiasis were obtained from publicly available datasets, including European-ancestry cholelithiasis datasets from FinnGen and GCST90044196. The inverse variance weighted method was used as the primary MR analysis, with complementary and sensitivity analyses performed to assess the robustness of the findings. Multivariable and mediation MR analyses were performed to evaluate whether inflammatory proteins mediated the pathway from cathepsins to cholelithiasis.ResultsAfter correction for multiple testing, genetically predicted cathepsin B was associated with an increased risk of cholelithiasis. Mediation analyses suggested that part of the effect of cathepsin B on cholelithiasis may be mediated by fibroblast growth factor 19 (FGF19) and interleukin-6 levels. In the reverse MR analysis, genetically predicted cholelithiasis showed potential associations with two cathepsins and twelve inflammatory proteins.ConclusionsThis MR study provides genetic evidence for a potential association between cathepsin B and increased cholelithiasis risk. FGF19 and interleukin-6 may serve as partial mediators in this association. - Source: PubMed
Publication date: 2026/08/01
Yuan TongWang Ting