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FGF19 is induced by hypoxia/reoxygenation (H/R) - treatment in cardiomyocytes. FGF19 knockdown augments H/R-induced injury. FGF19 overexpression protects cardiomyocytes from H/R-induced injury.
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Study shows that FXR is phosphorylated at Y67 by non-receptor tyrosine kinase, Src, in response to postprandial FGF19 which is critical for its nuclear localization and transcriptional regulation of bile acids levels and identifies Src-mediated FXR phosphorylation as a potential therapeutic target and biomarker for bile acids-related enterohepatic diseases.
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In children and adolescents with NAFLD, hepatic FXR protein content and plasma FGF19 concentrations were decreased compared.
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Study showed that FGF19 amplification is a genetic event in Chinese lung squamous cell carcinoma (LSCC) patients, with a frequency of 37.5%. FGF19 amplified LSCC cells express relatively higher levels of FGF19 mRNA expression, and downregulation of FGF19 expression can induce significant cell killing effects in vitro and in vivo.
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FGFR4/FGF19 autocrine signaling mediates the survival of a subset of basal-like breast cancer cells
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FGF19 copy number may increase in hepatocellular carcinoma accompanying a complete response to sorafenib treatment
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Study demonstrates that elevated FGF19 expression or hyperactivation of FGF19/FGFR4 signaling in hepatocellular carcinoma cells is one of the main mechanisms of sorafenib resistance.
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This is the first study to elucidate FGF19/FGFR4 signaling in favor of hepatocellular carcinoma cells developing from fatty liver
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High expression of FGF19 is associated with hepatocellular carcinoma.
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Findings show that FGF19 provides a cytoprotective role against ER stress by activating a FGFR4-GSK3beta-Nrf2 signaling cascade, suggesting targeting this signaling node as a candidate therapeutic regimen for hepatocellular carcinoma (HCC) management.
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Fibroblast growth factor 19 levels in human portal blood are higher than in arterial blood. Fibroblast growth factor 19 is released by the portal-drained viscera under fasted steady state conditions.
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Intestinal sensing of highly elevated levels of conjugated bile acids in blood promotes FGF15/FGF19 signaling, reducing hepatic bile acid synthesis and modulating bile acid transporters.
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serum FGF19 and FGF21 and hepatic Klotho expression are inversely associated with hepatic damage in children with NAFLD
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Administering FGF19, or suitable mimetic, as a pharmacological intervention to increase circulating levels of FGF19 and suppress BA synthesis by inhibiting CYP7A1 gene expression is likely to provide therapeutic benefits for many PBC patients
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Amplification of FGF19 was validated in independent LSCC samples. Furthermore, FGF19 stimulated LSCC cell growth in vitro. These data implicate FGF19 as a potential driver gene in LSCC with clinic characteristics as smoking.
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FGF19 is able to enhance migration and invasion abilities of gastric cancer cells.
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Bile acid and FGF19 levels increased after Roux-en-Y bypass, but not after intensive medial management in type 2 diabetic subjects who achieved similar improvement in glycemic control.
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FGF19 correlates with severity of liver disease and can potentially serve as an indicator of chronic cholestatic liver injury.
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Study shows that FGF19 can be secreted and promotes ovarian cancer progression such as proliferation and invasion by activating FGFR4.
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we suggest that considerable mechanistic differences exist between humans and mice with regard to the nuclear receptors controlling the VitA-FGF15/19 axis.
