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Gene Information

Gene symbol: FGFR2

Gene name: fibroblast growth factor receptor 2

HGNC ID: 3689

Synonyms: CEK3, TK14, TK25, ECT1, K-SAM, CD332

Related Genes

# Gene Symbol Number of hits
1 BAX 1 hits
2 BCL2 1 hits
3 BDNF 1 hits
4 BIRC5 1 hits
5 CDKN2A 1 hits
6 CLPS 1 hits
7 CRS 1 hits
8 EGFR 1 hits
9 ERBB2 1 hits
10 ERBB3 1 hits
11 ETS1 1 hits
12 EXOC7 1 hits
13 FGF1 1 hits
14 FGF10 1 hits
15 FGF19 1 hits
16 FGF2 1 hits
17 FGF21 1 hits
18 FGF23 1 hits
19 FGF4 1 hits
20 FGF5 1 hits
21 FGF7 1 hits
22 FGF8 1 hits
23 FGFR1 1 hits
24 FGFR3 1 hits
25 FGFR4 1 hits
26 FOS 1 hits
27 FRS2 1 hits
28 HRAS 1 hits
29 IGF1 1 hits
30 IGF1R 1 hits
31 INS 1 hits
32 INSR 1 hits
33 JUN 1 hits
34 KDR 1 hits
35 KIT 1 hits
36 KL 1 hits
37 MAPK1 1 hits
38 MAPK3 1 hits
39 MKI67 1 hits
40 MYC 1 hits
41 NCAM1 1 hits
42 NGFR 1 hits
43 NR1H4 1 hits
44 NRAS 1 hits
45 NTRK1 1 hits
46 NUDT6 1 hits
47 PDGFB 1 hits
48 PDGFRA 1 hits
49 PDGFRB 1 hits
50 PLA2G1B 1 hits
51 PPARG 1 hits
52 PSIP1 1 hits
53 PVR 1 hits
54 SLC2A4 1 hits
55 TP53 1 hits
56 VEGFA 1 hits

Related Sentences

# PMID Sentence
1 1645359 The basic fibroblast growth factor-saporin mitotoxin acts through the basic fibroblast growth factor receptor.
2 1645359 We have confirmed the hypothesis that a mitotoxin resulting from the conjugation of basic fibroblast growth factor and saporin exerts its cytotoxic effect through specific interaction with the basic fibroblast growth factor (FGF) receptor.
3 1645359 The basic fibroblast growth factor-saporin mitotoxin acts through the basic fibroblast growth factor receptor.
4 1645359 We have confirmed the hypothesis that a mitotoxin resulting from the conjugation of basic fibroblast growth factor and saporin exerts its cytotoxic effect through specific interaction with the basic fibroblast growth factor (FGF) receptor.
5 2165003 We recently characterized a specific cytotoxin to cells expressing the basic fibroblast growth factor receptor by conjugating the growth factor to saporin-6, a ribosome-inactivating protein.
6 2174511 Although it is known that the virion uses a basic fibroblast growth factor (FGF) receptor to penetrate vascular cells, it is not known how the viral particle recognizes and binds to this cell surface protein.
7 8090787 We have purified three acidic (FGF-1) and basic (FGF-2) fibroblast growth factor binding proteins (FGF-BP1, FGF-BP2, and FGF-BP3) from human plasma and calf serum and demonstrate the presence of these circulating FGF-BPs in blood.
8 8090787 Each are truncated forms of the high-affinity FGF receptor (FGFR-1).
9 8090787 FGF-BP1 and FGF-BP2 have estimated molecular masses of 70-85 kDa and 55-60 kDa, respectively, and are detected by using 125I-labeled FGF-2 ligand blotting.
10 8090787 Immunoblotting with four distinct antibodies to FGFR-1 reveals that FGF-BP1 and FGF-BP2 are immunologically and biochemically related to the extracellular domain of FGFR-1.
11 8090787 Protein sequencing of the amino terminus of FGF-BP2 and FGF-BP3 reveals identity with the extracellular domain of the two-IgG-loop form of human FGFR-1.
12 8214586 Basic fibroblast growth factor-saporin (FGF-SAP) is an extremely potent cytotoxic agent for cells bearing the FGF receptor.
13 8416827 Single-stranded RNA probes for the three chicken fibroblast growth factor (FGF) receptors, cek-1, cek-2, and cek-3, in conjunction with in situ hybridization were used to characterize the distribution of the corresponding mRNAs in the developing chicken embryo.
14 8416827 Cek-1 was expressed diffusely in most tissues examined, whereas the expression of cek-2 and cek-3 was more restricted.
15 8416827 Single-stranded RNA probes for the three chicken fibroblast growth factor (FGF) receptors, cek-1, cek-2, and cek-3, in conjunction with in situ hybridization were used to characterize the distribution of the corresponding mRNAs in the developing chicken embryo.
16 8416827 Cek-1 was expressed diffusely in most tissues examined, whereas the expression of cek-2 and cek-3 was more restricted.
17 9237137 Basic fibroblast growth factor mRNA, bFGF peptide and FGF receptor in epiretinal membranes of intraocular proliferative disorders (PVR and PDR).
18 9237137 Basic fibroblast growth factor (bFGF) has been shown to be involved in epiretinal membrane formation in proliferative vitreoretinal disorders.
19 9237137 We examined 20 epiretinal membranes from patients with proliferative diabetic retinopathy (PDR) (n = 12) and proliferative vitreoretinopathy (PVR) (n = 8) for the presence of bFGF peptide, fibroblast growth factor receptor-1 (FGFR-1) and bFGF messenger ribonucleic acid (mRNA).
20 9435295 Fibroblast growth factor receptor 2 (FGFR2)-mediated reciprocal regulation loop between FGF8 and FGF10 is essential for limb induction.
21 9435295 Consistent with this defect, the expression of Fgf8, an apical ectodermal factor, is absent in the mutant presumptive limb ectoderm, and the expression of Fgf10, a mesenchymally expressed limb bud initiator, is down regulated in the underlying mesoderm.
22 9435295 These findings provide direct genetic evidence that FGF/FGFR2 signals are absolutely required for vertebrate limb induction and that an FGFR2 signal is essential for the reciprocal regulation loop between FGF8 and FGF10 during limb induction.
23 9435295 Fibroblast growth factor receptor 2 (FGFR2)-mediated reciprocal regulation loop between FGF8 and FGF10 is essential for limb induction.
24 9435295 Consistent with this defect, the expression of Fgf8, an apical ectodermal factor, is absent in the mutant presumptive limb ectoderm, and the expression of Fgf10, a mesenchymally expressed limb bud initiator, is down regulated in the underlying mesoderm.
25 9435295 These findings provide direct genetic evidence that FGF/FGFR2 signals are absolutely required for vertebrate limb induction and that an FGFR2 signal is essential for the reciprocal regulation loop between FGF8 and FGF10 during limb induction.
26 9716527 FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
27 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.
28 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.
29 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.
30 9716527 These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
31 9755596 This study was undertaken to biochemically and immunohistochemically clarify the expression of basic fibroblast growth factor (bFGF), insulin-like growth factor-I (IGF-I), fibroblast growth factor receptor (bFGFR), insulin-like growth factor-I receptor (IGF-IR) and vascular smooth muscle cell (VSMC) growth by using Streptozotocin (STZ) treated rat serum.
32 9755596 Also according to western blot analysis, the protein synthesis of bFGFR and IGF-IR in the VSMCs was increased in STZ treated rat sera.
33 9755596 Immunohistochemically, bFGF, IGF-I and their receptors were much more localized in VSMCs in STZ treated rat sera than in control sera.
34 10748122 A novel type I fibroblast growth factor receptor activates mitogenic signaling in the absence of detectable tyrosine phosphorylation of FRS2.
35 10748122 A novel variant of the fibroblast growth factor receptor type 1 (FGFR-1) was identified in human placental RNA.
36 10748122 Transfected L6 clones expressed respective proteins and bound (125)I-labeled FGF-2 with K(d) values of 99 pm (FGFR-1) and 26 pm (FGFR-1L).
37 10748122 FGF-1 and FGF-2 competed efficiently with (125)I-FGF-2 for binding to FGFR-1 and FGFR-1L, whereas FGF-4 was less efficient.
38 10748122 FGF-1, FGF-2, and FGF-4 enhanced mitogen-activated protein kinase (MAPK) activity, increased steady-state c-fos mRNA levels, and stimulated proliferation through either receptor, whereas KGF was without effect.
39 10748122 FGFR-1 expressing clones exhibited ligand-induced tyrosine phosphorylation of fibroblast growth factor receptor substrate 2 (FRS2), a 90-kDa adaptor protein that links FGFR-1 activation to the MAPK cascade.
40 10748122 These findings indicate that FGFR-1L binds FGF-1 and FGF-2 with high affinity and is capable of mitogenic signaling, but may activate MAPK to occur via non-classical signaling intermediates.
41 10748122 A novel type I fibroblast growth factor receptor activates mitogenic signaling in the absence of detectable tyrosine phosphorylation of FRS2.
42 10748122 A novel variant of the fibroblast growth factor receptor type 1 (FGFR-1) was identified in human placental RNA.
43 10748122 Transfected L6 clones expressed respective proteins and bound (125)I-labeled FGF-2 with K(d) values of 99 pm (FGFR-1) and 26 pm (FGFR-1L).
44 10748122 FGF-1 and FGF-2 competed efficiently with (125)I-FGF-2 for binding to FGFR-1 and FGFR-1L, whereas FGF-4 was less efficient.
45 10748122 FGF-1, FGF-2, and FGF-4 enhanced mitogen-activated protein kinase (MAPK) activity, increased steady-state c-fos mRNA levels, and stimulated proliferation through either receptor, whereas KGF was without effect.
46 10748122 FGFR-1 expressing clones exhibited ligand-induced tyrosine phosphorylation of fibroblast growth factor receptor substrate 2 (FRS2), a 90-kDa adaptor protein that links FGFR-1 activation to the MAPK cascade.
47 10748122 These findings indicate that FGFR-1L binds FGF-1 and FGF-2 with high affinity and is capable of mitogenic signaling, but may activate MAPK to occur via non-classical signaling intermediates.
48 11130726 Here we show that the FGF receptors (FGFRs) 1 and 2, together with the ligands FGF1, FGF2, FGF4, FGF5, FGF7 and FGF10, are expressed in adult mouse beta-cells, indicating that FGF signalling may have a role in differentiated beta-cells.
49 11130726 We also show that Ipf1/Pdx1 is required for the expression of FGFR1 signalling components in beta-cells, indicating that Ipf1/Pdx1 acts upstream of FGFR1 signalling in beta-cells to maintain proper glucose sensing, insulin processing and glucose homeostasis.
50 11956156 Specifically, FGF23 is a regulator of serum inorganic phosphate levels, and mice deficient in FGF receptor-4 have altered cholesterol metabolism.
51 11956156 The recently described FGF19 is unusual in that it is nonmitogenic and appears to interact only with FGF receptor-4.
52 11956156 Specifically, FGF23 is a regulator of serum inorganic phosphate levels, and mice deficient in FGF receptor-4 have altered cholesterol metabolism.
53 11956156 The recently described FGF19 is unusual in that it is nonmitogenic and appears to interact only with FGF receptor-4.
54 12032663 Pancreatic ductal adenocarcinomas (PDACs) overexpress various cell-surface tyrosine kinase receptors, including the type I high-affinity fibroblast growth factor receptor (FGFR-1).
55 12032663 In parental L6 cells that express exceedingly low levels of high-affinity FGFRs, transduction with AdLuc was enhanced 7- to 10-fold with the FGF2-Fab' conjugate, whereas in L6 cells transfected to express FGFR-1, it was enhanced 39- to 52-fold.
56 12032663 In the absence of FGF2-Fab' there was no correlation between surface binding of FGF2 and AdLuc transduction efficiency, whereas in the presence of FGF2-Fab', enhanced AdLuc transduction efficiency correlated with greater surface binding of FGF2.
57 15199177 Inducible suppression of Fgfr2 and Survivin in ES cells using a combination of the RNA interference (RNAi) and the Cre-LoxP system.
58 15199177 We show that this system works with high efficiency in suppression of two endogenous genes, Fgfr2 and Survivin, in mouse embryonic stem (ES) cells, as evidenced by the decrease of levels of gene expression, reduced cell proliferation and colony formation.
59 15199177 Inducible suppression of Fgfr2 and Survivin in ES cells using a combination of the RNA interference (RNAi) and the Cre-LoxP system.
60 15199177 We show that this system works with high efficiency in suppression of two endogenous genes, Fgfr2 and Survivin, in mouse embryonic stem (ES) cells, as evidenced by the decrease of levels of gene expression, reduced cell proliferation and colony formation.
61 16186384 We have earlier shown that the fibroblast growth factor (FGF) receptor 2 is expressed in pancreatic progenitor cells and that FGF10, the high-affinity ligand of the FGF receptor 2 isoform FGF receptor 2b, promotes expansion of pancreatic progenitors.
62 16718462 IL-1beta-induced pro-apoptotic signalling is facilitated by NCAM/FGF receptor signalling and inhibited by the C3d ligand in the INS-1E rat beta cell line.
63 16840537 Fibroblast growth factor-2 (FGF-2) is a potent angiogenic factor and, according to previous evidence, may represent a key target of molecular modifications triggered by high-sugar exposure.
64 16840537 Under similar conditions, binding affinity to FGF receptor 1 was dramatically reduced by 20-fold, as well as FGF receptor 1 and ERK-1/2 phosphorylation, and FGF-2 lost about 45% of angiogenic activity in two different in vivo angiogenic (Matrigel and chorioallantoic-membrane) assays.
65 17063460 Molecular determinants of FGF-21 activity-synergy and cross-talk with PPARgamma signaling.
66 17063460 Here we describe the early signaling events triggered by FGF-21 treatment of 3T3-L1 adipocytes and reveal a functional interplay between FGF-21 and peroxisome proliferator-activated receptor gamma (PPARgamma) pathways that leads to a marked stimulation of glucose transport.
67 17063460 While the early actions of FGF-21 on 3T3-L1 adipocytes involve rapid accumulation of intracellular calcium and phosphorylation of Akt, GSK-3, p70(S6K), SHP-2, MEK1/2, and Stat3, continuous treatment for 72 h induces an increase in PPARgamma protein expression.
68 17063460 Moreover, chronic activation of the PPARgamma pathway in 3T3-L1 adipocytes with the PPARgamma agonist and anti-diabetic agent, rosiglitazone (BRL 49653), enhances FGF-21 action to induce tyrosine phosphorylation of FGF receptor-2.
69 17063460 Strikingly, treatment of cells with FGF-21 and rosiglitazone in combination leads to a pronounced increase in expression of the GLUT1 glucose transporter and a marked synergy in stimulation of glucose transport.
70 17063460 Together these results reveal a novel synergy between two regulators of glucose homeostasis, FGF-21 and PPARgamma, and further define FGF-21 mechanism of action.
71 17694057 Among them is Apert syndrome, one of the most severe forms of craniosynostosis, primarily caused by missense mutations leading to amino acid changes S252W or P253R in fibroblast growth factor receptor 2 (FGFR2).
72 17694057 Restoration of normal FGFR2 signaling is manifested by an alteration of the activity of extracellular signal-regulated kinases 1 and 2 (ERK1/2), implicating the gene encoding ERK and the genes downstream of it in disease expressivity.
73 17694057 Furthermore, treatment of the mutant mice with U0126, an inhibitor of mitogen-activated protein (MAP) kinase kinase 1 and 2 (MEK1/2) that blocks phosphorylation and activation of ERK1/2, significantly inhibits craniosynostosis.
74 17694057 These results illustrate a pathogenic role for ERK activation in craniosynostosis resulting from FGFR2 with the S252W substitution and introduce a new concept of small-molecule inhibitor-mediated prevention and therapy for diseases caused by gain-of-function mutations in the human genome.
75 17694057 Among them is Apert syndrome, one of the most severe forms of craniosynostosis, primarily caused by missense mutations leading to amino acid changes S252W or P253R in fibroblast growth factor receptor 2 (FGFR2).
76 17694057 Restoration of normal FGFR2 signaling is manifested by an alteration of the activity of extracellular signal-regulated kinases 1 and 2 (ERK1/2), implicating the gene encoding ERK and the genes downstream of it in disease expressivity.
77 17694057 Furthermore, treatment of the mutant mice with U0126, an inhibitor of mitogen-activated protein (MAP) kinase kinase 1 and 2 (MEK1/2) that blocks phosphorylation and activation of ERK1/2, significantly inhibits craniosynostosis.
78 17694057 These results illustrate a pathogenic role for ERK activation in craniosynostosis resulting from FGFR2 with the S252W substitution and introduce a new concept of small-molecule inhibitor-mediated prevention and therapy for diseases caused by gain-of-function mutations in the human genome.
79 17694057 Among them is Apert syndrome, one of the most severe forms of craniosynostosis, primarily caused by missense mutations leading to amino acid changes S252W or P253R in fibroblast growth factor receptor 2 (FGFR2).
80 17694057 Restoration of normal FGFR2 signaling is manifested by an alteration of the activity of extracellular signal-regulated kinases 1 and 2 (ERK1/2), implicating the gene encoding ERK and the genes downstream of it in disease expressivity.
81 17694057 Furthermore, treatment of the mutant mice with U0126, an inhibitor of mitogen-activated protein (MAP) kinase kinase 1 and 2 (MEK1/2) that blocks phosphorylation and activation of ERK1/2, significantly inhibits craniosynostosis.
82 17694057 These results illustrate a pathogenic role for ERK activation in craniosynostosis resulting from FGFR2 with the S252W substitution and introduce a new concept of small-molecule inhibitor-mediated prevention and therapy for diseases caused by gain-of-function mutations in the human genome.
83 18165258 Among the nitrated proteins were insulin-responsive glucose transporter type 4 (GLUT-4), which has been implicated previously in the pathogenesis of diabetes mellitus; exocyst complex component Exo70, which functions in insulin-stimulated glucose uptake of GLUT-4-containing vesicles; and fibroblast growth factor receptor 2, which influences retinal vascularization via fibroblast growth factor signaling.
84 18165258 Nitration of tyrosine phosphorylation sites were identified in five proteins, including GLUT-4, exocyst complex component Exo70, protein-tyrosine phosphatase eta, sensory neuron synuclein, and inositol trisphosphate receptor 3.
85 18225590 The expression of EGFR, erbB2, erbB3, FGFR-2, FGFR-3, c-myc, N-ras, ets-1, H-ras, c-fos and c-jun, the tumor suppressor genes p53 and p16, apoptosis markers Bax and Bcl-2, and the cell proliferation marker Ki-67 in the sequential stages of rat oral oncogenesis was investigated.
86 18225590 Diabetes seems to promote the activation of the Ras/Raf/MAPK signal transduction pathway mainly by induction of erbB2 and erbB3 receptors, leading to increased cell proliferation, while there was no difference in apoptosis levels during oncogenesis.
87 19237543 FGF15/FGFR4 integrates growth factor signaling with hepatic bile acid metabolism and insulin action.
88 19237543 The current studies show FGF15 signaling decreases hepatic forkhead transcription factor 1 (FoxO1) activity through phosphatidylinositol (PI) 3-kinase-dependent phosphorylation.
89 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.
90 19237543 Because FoxO1 activity and CYP7A1 gene expression are both increased by fasting, we hypothesized CYP7A1 might be a FoxO1 target gene.
91 19237543 Consistent with recently reported results, we show CYP7A1 is a direct target of FoxO1.
92 19237543 FGFR4 is the major hepatic FGF receptor isoform and is responsible for the hepatic effects of FGF15.
93 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.
94 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.
95 19346330 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).
96 19346330 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.
97 19346330 However, the mechanism by which FXR/FGF19/FGFR4 signaling inhibits CYP7A1 remains unknown.
98 19577003 In particular, significant overexpressions of colipase, phospholipase A2, carboxypeptidases, and receptor tyrosine kinases such as EGFR, erbB2 and fibroblast growth factor receptor were observed in diabetes mesenteric vasculature.
99 21177529 The cooperation of FGF receptor and Klotho is involved in excretory canal development and regulation of metabolic homeostasis in Caenorhabditis elegans.
100 22174314 Here, we describe an alternative antidiabetic strategy using agonistic anti-FGFR1 (FGF receptor 1) antibodies (R1MAbs) that mimic the metabolic effects of FGF21.
101 22174314 In brown adipose tissues, both FGF21 and R1MAb induced phosphorylation of CREB (cyclic adenosine 5'-monophosphate response element-binding protein), and mRNA expression of PGC-1α (peroxisome proliferator-activated receptor-γ coactivator 1α) and the downstream genes associated with oxidative metabolism.
102 22174314 Collectively, we propose FGFR1 in adipose tissues as a major functional receptor for FGF21, as an upstream regulator of PGC-1α, and as a compelling target for antibody-based therapy for type 2 diabetes and other obesity-associated disorders.
103 23197570 As an alternative to native FGF21, we have developed a monoclonal antibody, mimAb1, that binds to βKlotho with high affinity and specifically activates signaling from the βKlotho/FGFR1c (FGF receptor 1c) receptor complex.
104 23197570 In obese cynomolgus monkeys, injection of mimAb1 led to FGF21-like metabolic effects, including decreases in body weight, plasma insulin, triglycerides, and glucose during tolerance testing.
105 23197570 Mice with adipose-selective FGFR1 knockout were refractory to FGF21-induced improvements in glucose metabolism and body weight.
106 23197570 These results in obese monkeys (with mimAb1) and in FGFR1 knockout mice (with FGF21) demonstrated the essential role of FGFR1c in FGF21 function and suggest fat as a critical target tissue for the cytokine and antibody.
107 23577003 We have provided an overview of functional BRET studies associated with the RTK superfamily involving: neurotrophic receptors [e.g., tropomyosin-related kinase (Trk) and p75 neurotrophin receptor (p75NTR)]; insulinotropic receptors [e.g., insulin receptor (IR) and insulin-like growth factor receptor (IGFR)] and growth factor receptors [e.g., ErbB receptors including the EGFR, the fibroblast growth factor receptor (FGFR), the vascular endothelial growth factor receptor (VEGFR) and the c-kit and platelet-derived growth factor receptor (PDGFR)].
108 23577003 In addition, we review BRET-mediated studies of other tyrosine kinase-associated receptors including cytokine receptors, i.e., leptin receptor (OB-R) and the growth hormone receptor (GHR).