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PMID |
Sentence |
1 |
9703323
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FGFR1 and FGFR4 were shown to be expressed at a high level during early pancreatic development before embryonic day 16, their levels of expression decreasing thereafter.
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2 |
9703323
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It was demonstrated in vitro that both FGF1 and FGF2 induce the expression of NGFI-A mRNA, a useful indicator of functional growth factor-signaling pathways.
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3 |
9703323
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Finally, the effect of FGF2 on embryonic pancreatic epithelial cell proliferation was studied.
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4 |
9703323
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It was shown that FGF2 induces the proliferation of pancreatic epithelial cells during embryonic life.
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5 |
9716527
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FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
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6 |
9716527
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An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
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7 |
9716527
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However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
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8 |
9716527
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Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
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9 |
9716527
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These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
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10 |
9716527
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FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
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11 |
9716527
|
An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
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12 |
9716527
|
However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
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13 |
9716527
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Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
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14 |
9716527
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These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
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15 |
9716527
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FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
|
16 |
9716527
|
An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
|
17 |
9716527
|
However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
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18 |
9716527
|
Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
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19 |
9716527
|
These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
|
20 |
9716527
|
FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
|
21 |
9716527
|
An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
|
22 |
9716527
|
However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
|
23 |
9716527
|
Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
|
24 |
9716527
|
These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
|
25 |
9716527
|
FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
|
26 |
9716527
|
An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
|
27 |
9716527
|
However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
|
28 |
9716527
|
Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
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29 |
9716527
|
These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
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30 |
19237543
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FGF15/FGFR4 integrates growth factor signaling with hepatic bile acid metabolism and insulin action.
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31 |
19237543
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The current studies show FGF15 signaling decreases hepatic forkhead transcription factor 1 (FoxO1) activity through phosphatidylinositol (PI) 3-kinase-dependent phosphorylation.
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32 |
19237543
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The bile acid receptor FXR (farnesoid X receptor) activates expression of fibroblast growth factor (FGF) 15 in the intestine, which acts through hepatic FGFR4 to suppress cholesterol-7alpha hydroxylase (CYP7A1) and limit bile acid production.
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33 |
19237543
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Because FoxO1 activity and CYP7A1 gene expression are both increased by fasting, we hypothesized CYP7A1 might be a FoxO1 target gene.
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34 |
19237543
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Consistent with recently reported results, we show CYP7A1 is a direct target of FoxO1.
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35 |
19237543
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FGFR4 is the major hepatic FGF receptor isoform and is responsible for the hepatic effects of FGF15.
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36 |
19237543
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We also show that expression of FGFR4 in liver was decreased by fasting, increased by insulin, and reduced by streptozotocin-induced diabetes, implicating FGFR4 as a primary target of insulin regulation.
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37 |
19237543
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Because insulin and FGF both target the PI 3-kinase pathway, these observations suggest FoxO1 is a key node in the convergence of FGF and insulin signaling pathways and functions as a key integrator for the regulation of glucose and bile acid metabolism.
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38 |
19237543
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FGF15/FGFR4 integrates growth factor signaling with hepatic bile acid metabolism and insulin action.
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39 |
19237543
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The current studies show FGF15 signaling decreases hepatic forkhead transcription factor 1 (FoxO1) activity through phosphatidylinositol (PI) 3-kinase-dependent phosphorylation.
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40 |
19237543
|
The bile acid receptor FXR (farnesoid X receptor) activates expression of fibroblast growth factor (FGF) 15 in the intestine, which acts through hepatic FGFR4 to suppress cholesterol-7alpha hydroxylase (CYP7A1) and limit bile acid production.
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41 |
19237543
|
Because FoxO1 activity and CYP7A1 gene expression are both increased by fasting, we hypothesized CYP7A1 might be a FoxO1 target gene.
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42 |
19237543
|
Consistent with recently reported results, we show CYP7A1 is a direct target of FoxO1.
|
43 |
19237543
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FGFR4 is the major hepatic FGF receptor isoform and is responsible for the hepatic effects of FGF15.
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44 |
19237543
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We also show that expression of FGFR4 in liver was decreased by fasting, increased by insulin, and reduced by streptozotocin-induced diabetes, implicating FGFR4 as a primary target of insulin regulation.
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45 |
19237543
|
Because insulin and FGF both target the PI 3-kinase pathway, these observations suggest FoxO1 is a key node in the convergence of FGF and insulin signaling pathways and functions as a key integrator for the regulation of glucose and bile acid metabolism.
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46 |
19237543
|
FGF15/FGFR4 integrates growth factor signaling with hepatic bile acid metabolism and insulin action.
|
47 |
19237543
|
The current studies show FGF15 signaling decreases hepatic forkhead transcription factor 1 (FoxO1) activity through phosphatidylinositol (PI) 3-kinase-dependent phosphorylation.
|
48 |
19237543
|
The bile acid receptor FXR (farnesoid X receptor) activates expression of fibroblast growth factor (FGF) 15 in the intestine, which acts through hepatic FGFR4 to suppress cholesterol-7alpha hydroxylase (CYP7A1) and limit bile acid production.
|
49 |
19237543
|
Because FoxO1 activity and CYP7A1 gene expression are both increased by fasting, we hypothesized CYP7A1 might be a FoxO1 target gene.
|
50 |
19237543
|
Consistent with recently reported results, we show CYP7A1 is a direct target of FoxO1.
|
51 |
19237543
|
FGFR4 is the major hepatic FGF receptor isoform and is responsible for the hepatic effects of FGF15.
|
52 |
19237543
|
We also show that expression of FGFR4 in liver was decreased by fasting, increased by insulin, and reduced by streptozotocin-induced diabetes, implicating FGFR4 as a primary target of insulin regulation.
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53 |
19237543
|
Because insulin and FGF both target the PI 3-kinase pathway, these observations suggest FoxO1 is a key node in the convergence of FGF and insulin signaling pathways and functions as a key integrator for the regulation of glucose and bile acid metabolism.
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54 |
19237543
|
FGF15/FGFR4 integrates growth factor signaling with hepatic bile acid metabolism and insulin action.
|
55 |
19237543
|
The current studies show FGF15 signaling decreases hepatic forkhead transcription factor 1 (FoxO1) activity through phosphatidylinositol (PI) 3-kinase-dependent phosphorylation.
|
56 |
19237543
|
The bile acid receptor FXR (farnesoid X receptor) activates expression of fibroblast growth factor (FGF) 15 in the intestine, which acts through hepatic FGFR4 to suppress cholesterol-7alpha hydroxylase (CYP7A1) and limit bile acid production.
|
57 |
19237543
|
Because FoxO1 activity and CYP7A1 gene expression are both increased by fasting, we hypothesized CYP7A1 might be a FoxO1 target gene.
|
58 |
19237543
|
Consistent with recently reported results, we show CYP7A1 is a direct target of FoxO1.
|
59 |
19237543
|
FGFR4 is the major hepatic FGF receptor isoform and is responsible for the hepatic effects of FGF15.
|
60 |
19237543
|
We also show that expression of FGFR4 in liver was decreased by fasting, increased by insulin, and reduced by streptozotocin-induced diabetes, implicating FGFR4 as a primary target of insulin regulation.
|
61 |
19237543
|
Because insulin and FGF both target the PI 3-kinase pathway, these observations suggest FoxO1 is a key node in the convergence of FGF and insulin signaling pathways and functions as a key integrator for the regulation of glucose and bile acid metabolism.
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62 |
19346330
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In the liver, bile acids activate a nuclear receptor, farnesoid X receptor (FXR), that induces an atypical nuclear receptor small heterodimer partner, which subsequently inhibits nuclear receptors, liver-related homolog-1, and hepatocyte nuclear factor 4alpha and results in inhibiting transcription of the critical regulatory gene in bile acid synthesis, cholesterol 7alpha-hydroxylase (CYP7A1).
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63 |
19346330
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In the intestine, FXR induces an intestinal hormone, fibroblast growth factor 15 (FGF15; or FGF19 in human), which activates hepatic FGF receptor 4 (FGFR4) signaling to inhibit bile acid synthesis.
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64 |
19346330
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However, the mechanism by which FXR/FGF19/FGFR4 signaling inhibits CYP7A1 remains unknown.
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65 |
19346330
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In the liver, bile acids activate a nuclear receptor, farnesoid X receptor (FXR), that induces an atypical nuclear receptor small heterodimer partner, which subsequently inhibits nuclear receptors, liver-related homolog-1, and hepatocyte nuclear factor 4alpha and results in inhibiting transcription of the critical regulatory gene in bile acid synthesis, cholesterol 7alpha-hydroxylase (CYP7A1).
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66 |
19346330
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In the intestine, FXR induces an intestinal hormone, fibroblast growth factor 15 (FGF15; or FGF19 in human), which activates hepatic FGF receptor 4 (FGFR4) signaling to inhibit bile acid synthesis.
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67 |
19346330
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However, the mechanism by which FXR/FGF19/FGFR4 signaling inhibits CYP7A1 remains unknown.
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68 |
20157585
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Role of FGF19 induced FGFR4 activation in the regulation of glucose homeostasis.
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69 |
20157585
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FGF19, FGF21, and FGF23 form a unique subfamily of fibroblast growth factors.
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70 |
20157585
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FGF23 and its co-receptor alphaKlotho are involved in the control of aging, but it is not known if the same holds true for FGF19, which can also signal through alphaKlotho.
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71 |
20157585
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We have recently fully characterized FGF19/FGFR/co-factor interactions and signaling, and in the current manuscript discuss the contribution of the FGF19/FGFR4 axis to bile acid and glucose regulation.
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72 |
20157585
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Role of FGF19 induced FGFR4 activation in the regulation of glucose homeostasis.
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73 |
20157585
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FGF19, FGF21, and FGF23 form a unique subfamily of fibroblast growth factors.
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74 |
20157585
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FGF23 and its co-receptor alphaKlotho are involved in the control of aging, but it is not known if the same holds true for FGF19, which can also signal through alphaKlotho.
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75 |
20157585
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We have recently fully characterized FGF19/FGFR/co-factor interactions and signaling, and in the current manuscript discuss the contribution of the FGF19/FGFR4 axis to bile acid and glucose regulation.
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76 |
22442730
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Differential specificity of endocrine FGF19 and FGF21 to FGFR1 and FGFR4 in complex with KLB.
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77 |
23747238
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A polymorphism in the fibroblast growth factor receptor 4 gene has been associated with cancer progression and treatment resistance and is now reported to increase insulin secretion, providing a possible genetic link between hyperinsulinemia and cancer (Ezzat et al., 2013).
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78 |
23747250
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This STAT activation transcriptionally induces Grb14 in pancreatic endocrine cells to promote insulin secretion.
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79 |
23747250
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Knockin mice with the FGFR4 variant allele develop pancreatic islets that secrete more insulin, a feature that is reversed through Grb14 deletion and enhanced with FGF19 administration.
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