ライフサイエンスコーパス: FGFR2

1 cally targeted genes (e.g. PIK3CA, ERBB2 and FGFR2).

2 lele of fibroblast growth factor receptor 2 (FGFR2).

3 site on fibroblast growth factor receptor 2 (FGFR2).

4 way members and the receptor tyrosine kinase FGFR2.

5 NSCLC driven by a kinase domain mutation in FGFR2.

6 s a more prominent role in this process than FGFR2.

7 and with variants in AXIN2, FGF3, FGF10, and FGFR2.

8 ing a risk haplotype in the second intron of FGFR2.

9 into the hydrophobic transmembrane domain of FGFR2.

10 x genes, and at previously published SNPs of FGFR2.

11 in, with Fgfr1 being a stronger inducer than Fgfr2.

12 total of 11 SNPs from eight genomic regions (FGFR2, 9q31.2, MAP3K, CCND1, ZM1Z1, RAD51L11, ESR1 and U

13 Moreover, signaling through FGFR2, a known risk factor in breast cancer development,

14 Phosphorylation of Grb2 by FGFR2 abrogated its binding to the receptor, resulting i

15 n BBDS, which amplify nucleolar targeting of FGFR2, activate ribosomal DNA (rDNA) transcription and d

16 Nucleolar FGFR2 activates rDNA transcription via interactions with

17 We demonstrate that the mechanism of FGFR2 activation and subsequent transformation is mediat

18 a mechanism is described in which control of FGFR2 activation is provided by the adaptor protein Grb2

19 tion system in ES cells, we demonstrate that FGFR2 activation rapidly down-regulated Nanog gene trans

20 rethra are controlled by discrete regions of Fgfr2 activity.

21 and development of VUR and the mechanisms of Fgfr2 activity.

22 Here, we investigated whether Fgfr2 acts specifically in peri-Wolffian duct stroma (ST

23 In FGFR2-expressing cancer cell lines, this FGFR2-ADC exhibited potency in the low nanomolar to subn

24 Efficacy studies demonstrated that FGFR2-ADC treatment leads to a significant tumor growth

25 s indicated that the toxophore metabolite of FGFR2-ADC was enriched more than 30-fold in tumors compa

26 tubule-disrupting cytotoxic drug auristatin (FGFR2-ADC).

27 r, the increased risk conferred by the minor FGFR2 allele associates most strongly in oestrogen recep

28 and fibroblast growth factor receptor gene (FGFR2), among others.

29 Furthermore, FGFR2 amplification or mRNA overexpression predicted hig

30 ng mutations in the tyrosine kinase receptor FGFR2, analogous to those reported in ovarian and endome

31 found ligand-independent phosphorylation of FGFR2 and activation of p38 signaling in mutant skin and

32 n epithelial progenitors, showing that Sox9, Fgfr2 and Fgf10 form a feed-forward expression loop in t

33 he oncogenic nature of mutations observed in FGFR2 and FGFR3, each of which are observed in 3% of sam

34 ve genes (fibroblast growth factor receptors FGFR2 and FGFR3, tyrosine phosphatase PTPN11, and RAS on

35 mediate at least in part the signaling from FGFR2 and FGFR3.

36 Mice with ureteric deletion of both Fgfr2 and Frs2alpha (Fgfr2/Frs2alpha(UB-/)) were compare

37 Taken together, although Fgfr2 and Frs2alpha have crucial roles in the ureteric l

38 FGF10 is an oncogene that binds to FGFR2 and is overexpressed in approximately 10% of human

39 electively reduced plasma-membrane levels of FGFR2 and markedly diminished the receptor's responsiven

40 FGFR2 and other FGFR kinase family gene alterations have

41 Our results indicate that FGFR2 and PAPSS2 may play an important role in the regul

42 Both reciprocal activities of FGFR2 and Shp2 were inhibited by binding of Grb2 to the

43 ol over the mutually dependent activities of FGFR2 and Shp2.

44 he fibroblast growth factor receptor 2 gene (FGFR2) and the TOC high mobility group box family member

45 FGF receptor (FGFR) KO mice; however, FGFR1, FGFR2, and FGFR3 KO mice did not mimic the phenotype of

46 ee fibroblast growth factor receptors-FGFR1, FGFR2, and FGFR3-in the absence of ligand.

47 kely receptor mediated, albeit not by FGFR1, FGFR2, and FGFR3.

48 etable mutations in SMO, DDR2, FGFR1, PTCH1, FGFR2, and MET Our results indicate that a significant p

49 neurons, while its main receptors FGFR1 and FGFR2 are expressed by cortical projection neurons.

50 Somatic mutations in FGFR2 are present in 4% to 5% of patients diagnosed with

51 FGF receptors 1 and 2 (Fgfr1 and Fgfr2) are both expressed in the osteoprogenitor lineage

52 Identifying FGFR2 as a transcriptional regulator of rDNA in bone une

53 ased hepatic expression of FGF10, FGFR1, and FGFR2 as well as mesenchymal genes SLUG and SNAIL.

54 within fibroblast growth factor receptor 2 (FGFR2) as one of the highest ranking risk alleles in ter

55 They also provide the stem cell regulator, FGFR2, as a promising candidate target for future SS the

56 the fibroblast growth factor receptor gene, Fgfr2, as one occupied and upregulated by SYT-SSX2.

57 s to be driven largely by FGF5 activation of FGFR2, as siRNA silencing of this ligand or receptor, re

58 al signaling, enhance nucleolar occupancy of FGFR2 at the ribosomal DNA (rDNA) promoter.

59 Aberrant splicing of Fgfr2 blocked stria vascularis formation due to erroneou

60 ity of a neural crest enhancer downstream of FGFR2 both in vitro and in vivo.

61 tion of fibroblast growth factor receptor 2 (Fgfr2) broadly in renal and urinary tract mesenchyme led

62 aling, through cooperation between Fgfr1 and Fgfr2 but not Fgfr3, is required for the initial generat

63 s caused by mutations in the FGF receptor 2 (FGFR2), but the molecular mechanisms that induce skin an

64 petent avian sarcoma virus expressing either FgfR2(C278F), a receptor mutation found in Crouzon syndr

65 Significantly, deletion of FGFR2 caused a partial rescue of the Pten-null phenotype

66 Embryonic knockout of FGFR2 causes a reduction of hippocampal volume and impai

67 Mutations in FGFR2 could possibly cause VUR in humans.

68 Mechanistically, FGF23 binding to FGFR2 counteracted selectin- and chemokine-triggered bet

69 G1, TPM3-NTRK1 and RUFY2-RET in lung cancer, FGFR2-CREB5 in cholangiocarcinoma and PPL-NTRK1 in thyro

70 FGFR2 cycles between its kinase-active, partially phosph

71 wn to regulate myelin thickness, we examined FGFR2-deficient mice for the expression of key signaling

72 To test this hypothesis, we mated the Fgfr1-/Fgfr2-deficient mice with mast cell-deficient CreMaster

73 and degranulated in the skin of young Fgfr1-/Fgfr2-deficient mice, most likely as a consequence of in

74 Using Fgfr1-/Fgfr2-deficient mice, we analyzed the consequences of th

75 sults in two distinct phenotypes: endodermal Fgfr2 deletion causes mild hypospadias and inhibits matu

76 Fgfr2 deletion in the ocular surface epithelium reduced

77 Basal cells lacking Fgfr2 did not generate an epithelial network owing to a

78 Using an inducible FGFR2 dimerization system in ES cells, we demonstrate th

79 s are separate from previously characterized FGFR2 disorders and represent a distinct skeletal dyspla

80 We show that Fgfr1 and Fgfr2 double knockouts (FGFR DKO) generated by Cre-media

81 This is the first FGFR2-driven lung cancer GEMM, which can be applied acro

82 role of TRPA1 ankyrin repeats in regulating FGFR2-driven oncogenic process; a mechanism that is hind

83 ously established that the membrane receptor FGFR2 drives LUAD progression through aberrant protein-p

84 tion among patients with malocclusion, while FGFR2, EDN1, TBX5, and COL1A1 are associated with type o

85 lly targetable kinases such as ERBB2, FGFR1, FGFR2, EGFR, and MET, suggesting the potential use of ge

86 In FGFR2-expressing cancer cell lines, this FGFR2-ADC exhib

87 ll cell populations of the blastocyst, while Fgfr2 expression becomes restricted to extraembryonic li

88 f10 expression in the adjacent mesenchyme or Fgfr2 expression in the epithelium, but appeared to redu

89 We identify and characterize novel FGFR2 extracellular domain insertion mutations and demon

90 ion in fgf8 (fibroblast growth factor 8) and fgfr2 (fgf receptor 2) transcripts.

91 e or Tie2-Cre mediated deletion of FGFR1 and FGFR2 (Fgfr1/2(Flk1-Cre) or Fgfr1/2(Tie2-Cre) mice), whi

92 Conditional deletion of Fgfr1 and Fgfr2 from this tissue resulted in the formation of smal

93 wever, have normal kidneys; the roles of the Fgfr2/Frs2alpha signaling axis in MM development and reg

94 ken together, these results demonstrate that Fgfr2/Frs2alpha signaling in the MM promotes Bmp4 expres

95 eteric deletion of both Fgfr2 and Frs2alpha (Fgfr2/Frs2alpha(UB-/)) were compared with Frs2alpha(UB-/

96 At later stages, however, Fgfr2/Frs2alpha(UB-/-) kidneys were more severely affect

97 2(UB-/-) kidneys were indistinguishable from Fgfr2/Frs2alpha(UB-/-).

98 f a cohort of 107 iCCA patients reveals that FGFR2 fusions represent the most recurrent targetable al

99 t least one actionable molecular alteration (FGFR2 fusions, IDH1/2, ARAF, KRAS, BRAF and FGF19) that

100 eted therapeutically, such as fusions in the FGFR2 gene and mutations in genes encoding isocitrate de

101 Heterozygous mutations in the human FGFR2 gene cause various craniosynostosis syndromes incl

102 nt for breast cancer risk SNPs in the nearby FGFR2 gene, suggesting that TACC2 is a novel, independen

103 rs1219648, which annotates the FGFR2 gene, was associated with risk in both series (com

104 ephosphorylation of Grb2 by Shp2 rescued the FGFR2-Grb2 complex.

105 FGF receptor 2 (FGFR2) has a significant role in the production of corti

106 FGF-10 and its receptors, FGFR1 and FGFR2, have been implicated in breast cancer susceptibil

107 turn, inhibits TRPA1-mediated activation of FGFR2, hindering the metastatic process.

108 FR1c2 HS binding sites of the symmetric FGF2-FGFR2-HS2 signal transduction complex.

109 sette exons that generate receptor variants (FGFR2 IIIb or IIIc) with different ligand specificities.

110 ent with these tumor-suppressive properties, FGFR2-IIIb and FGFR2-IIIc each diminished invasive behav

111 the fibroblast growth factor (FGF) receptor FGFR2-IIIb and FGFR2-IIIc varying their extracellular st

112 1179470), which binds to the FGFR2 isoforms FGFR2-IIIb and FGFR2-IIIc, conjugated through a noncleav

113 Conversely, FGFR2-IIIb expression in epithelial cells yielded higher

114 Enforced expression of either FGFR2-IIIb or FGFR2-IIIc in thyroid epithelial cancer ce

115 tumor-suppressive properties, FGFR2-IIIb and FGFR2-IIIc each diminished invasive behavior in vitro an

116 Enforced expression of either FGFR2-IIIb or FGFR2-IIIc in thyroid epithelial cancer cells reduced ex

117 growth factor (FGF) receptor FGFR2-IIIb and FGFR2-IIIc varying their extracellular structure in huma

118 h binds to the FGFR2 isoforms FGFR2-IIIb and FGFR2-IIIc, conjugated through a noncleavable linker to

119 GF4/FGF7 expression that, in the presence of FGFR2-IIIc-expressing fibroblasts, enhanced tumor progre

120 Deletion of either Fgf9 or Fgfr2 in an XY gonad resulted in up-regulation of Wnt4 a

121 An increase in the nucleolar activity of FGFR2 in BBDS elevates levels of ribosomal RNA in the de

122 Knockdown of FGFR2 in both BMMSCs and SS cells abrogated their growth

123 981578, resulting in increased expression of FGFR2 in cancers from patients homozygous for that allel

124 High expression levels of FGFR2 in cells correlated with efficient internalization

125 pment by generating conditional deletions of Fgfr2 in each of these cell types.

126 required to maintain expression of Sox9 and Fgfr2 in epithelial progenitors, showing that Sox9, Fgfr

127 FGFR1 again having a greater influence than FGFR2 in ESC exit from the pluripotent state.

128 we investigate the tissue-specific roles of Fgfr2 in external genital development by generating cond

129 ther, these findings support a dual role for FGFR2 in hippocampal short-term learning and long-term r

130 Here, we have examined the requirement of Fgfr2 in mouse mammary gland morphogenesis using a postn

131 mice lacking both FGF receptor 1 (Fgfr1) and Fgfr2 in oligodendrocyte-lineage cells but found that in

132 We conditionally deleted Fgfr2 in ST (Fgfr2(ST-/-)) using Tbx18cre mice.

133 er, our data highlight a pleiotropic role of Fgfr2 in stem cell differentiation and branch initiation

134 vere hypospadias highlights a major role for Fgfr2 in the developing genital surface epithelium, wher

135 ciency or the targeted deletion of FGFR1 and FGFR2 in the hindlimb motor cortex limits the formation

136 Here we dissociate the role of FGFR2 in the hippocampus during development and during a

137 Deletion of Fgfr2 in the MM leads to kidneys with cranially displace

138 Unlike mice lacking both Fgfr1 and Fgfr2 in the MM, these mice had no obvious MM defects bu

139 in which FGFs, possibly from axons, activate FGFR2 in the oligodendrocyte/myelin compartment to incre

140 we show that specific deletion of Fgfr1 and Fgfr2 in the optic vesicle disrupts ERK signaling, which

141 ionally deleting one copy of FGF receptor 2 (FGFR2) in adult mouse airway basal cells results in self

142 ream of fibroblast growth factor receptor 2 (Fgfr2) in regulating early calvarial osteogenic differen

143 dysplasia syndrome (BBDS) demonstrates that FGFR2, in addition to its canonical signaling activities

144 These findings illustrate well how FGFR2 induces rapid but reversible Nanog repression with

145 bind to the C-terminal proline-rich motif of FGFR2 inducing the constitutive activation of the recept

146 a provide evidence that genetic variation in FGFR2 influences radiation-induced breast cancer risk.

147 g axis in endogenous SCCs using the clinical FGFR2 inhibitor AZD4547.

148 ich is successfully inhibited by a selective FGFR2 inhibitor in vitro.

149 We identified EFNB2, FGFR1, FGFR2, INSR, IRS2, NOTCH2, TLE1, and NTRK2 as novel mark

150 Here the authors propose that TRPA1/FGFR2 interaction is functional in LUAD and show that as

151 howed that the alternative splicing event of FGFR2 is associated with virus infection, tumor size, ci

152 We confirmed that Fgfr2 is expressed in ST and that Fgfr2 was efficiently

153 bryonic precursor of the penis and clitoris, Fgfr2 is expressed in two epithelial populations: the en

154 The fibroblast growth factor receptor FGFR2 is overexpressed in a variety of solid tumors, inc

155 779) in the cytoplasmic domains of FGFR1 and FGFR2 is required for the sustained activation of Ras an

156 The 10q26 locus in the second intron of FGFR2 is the locus most strongly associated with estroge

157 Fibroblast growth factor receptor 2 (FGFR2) is a crucial regulator of bone formation during e

158 Here, we show that FGF receptor type 2 (FGFR2) is highly enriched at the paranodal loops of myel

159 t ectopic expression of GATA6, together with FGFR2 isoform IIIb, increases anchorage-independent grow

160 tibody (mAb BAY 1179470), which binds to the FGFR2 isoforms FGFR2-IIIb and FGFR2-IIIc, conjugated thr

161 Despite the PrE-specific expression of FGFR2, it is FGFR1, expressed by all ICM cells, that is

162 even of nine Src family kinase genes, FGFR1, FGFR2, ITK, NTRK1, NTRK2, MOS, MST1R, and RAF1.

163 roblast growth factor receptor 1 (Fgfr1) and Fgfr2 (K5-R1/R2 mice) in the epidermis have a severe imp

164 d-independent dimerization and activation of FGFR2 kinase activity.

165 ch RTK, fibroblast growth factor receptor 2 (FGFR2) kinase, is still unknown, as the numerous crystal

166 alterations in ALK, ARAF, BRAF, EGFR, FGFR1, FGFR2, KIT, KRAS, MAP2K1, MET, NF1, NF2, NRAS, RAF1, RET

167 at mutations in the extracellular domains of FGFR2 lead to constitutive FGFR dimerization.

168 The associations at the FGFR2 locus were also weakly replicated in a dataset fro

169 The fibroblast growth factor receptor 2 (FGFR2) locus has been consistently identified as a breas

170 Furthermore, in vivo Fgfr2 loss-of-function in the ectoderm caused derepressi

171 al rescue of Fgfr1 forming heterodimers with Fgfr2(LR) alleles to recruit Frs2alpha, compound mutant

172 Fgfr1(Mes-/-)Fgfr2(LR/LR) mice also had subsequent defects in ureteri

173 d mice with both Fgfr1 deleted in the MM and Fgfr2(LR/LR) point mutations (Fgfr1(Mes-/-)Fgfrf2(LR/LR)

174 ted with ureteric deletion of Fgfr1 and with Fgfr2(LR/LR) point mutations (Fgfr1(UB-/-)Fgfr2(LR/LR)).

175 ding site for the docking protein Frs2alpha (Fgfr2(LR/LR)), however, have normal kidneys; the roles o

176 th Fgfr2(LR/LR) point mutations (Fgfr1(UB-/-)Fgfr2(LR/LR)).

177 -of-function studies in mice have shown that FGFR2 maintains a critical balance between the prolifera

178 Of interest, FGFR2-mediated Nanog transcriptional reduction occurred

179 However, the molecular mechanisms underlying FGFR2-mediated risk are still unknown.

180 d a preponderance of cancer genes, including FGFR2, MEN1, HOOK3, EZH2, MLF1, CARD11, VHL, NONO, and S

181 In contrast, in the asymmetric FGF2-HS1-FGFR2 model, a single HS chain interacts with the FGF2-F

182 In the symmetric FGF2-HS2-FGFR2 model, two acidic HS chains bind in a basic canyon

183 Dimeric Grb2 binds to the C termini of two FGFR2 molecules.

184 It consists of a fully human FGFR2 monoclonal antibody (mAb BAY 1179470), which binds

185 ssed the induction of HER3, InsR, IGF1R, and FGFR2 mRNAs upon inhibition of PI3K.

186 Second-line dovitinib in FGFR2(mut) and FGFR2(non-mut) advanced or metastatic end

187 ith FGFR2 prescreening results, 27 (11%) had FGFR2(mut) endometrial cancer.

188 Dec 13, 2013, we enrolled 22 patients in the FGFR2(mut) group and 31 patients in the FGFR2(non-mut) g

189 en (31.8%, 95% CI 13.9-54.9) patients in the FGFR2(mut) group and nine (29.0%, 14.2-48.0) in the FGFR

190 seven (35%) of the first 20 patients in the FGFR2(mut) group were progression free at 18 weeks, as w

191 s, as were five (25%) of the first 20 in the FGFR2(mut) population.

192 therapy both in patients with FGFR2-mutated (FGFR2(mut)) endometrial cancer and in those with FGFR2-n

193 ot the formation, of tetrads and rosettes in Fgfr2 mutant limb-bud ectoderm.

194 s reduced in the hypomyelinated CNS of Fgfr1/Fgfr2 mutant mice.

195 titutions: the C178S FGFR1 mutant, the C342R FGFR2 mutant, and the C228R FGFR3 mutant.

196 rapeutically targeting this unique subset of FGFR2-mutant cancers as well as insight into their oncog

197 Both FGFR2-mutant forms are predominantly located in the endo

198 f Wnt4 could rescue sex reversal in Fgf9 and Fgfr2 mutants.

199 as second-line therapy both in patients with FGFR2-mutated (FGFR2(mut)) endometrial cancer and in tho

200 In addition, we report a patient with an FGFR2-mutated oral SCC who responded to the multitargete

201 In summary, this study identifies the first FGFR2 mutation in a 46,XY GD patient.

202 We grouped women according to FGFR2 mutation status and gave all women dovitinib (500

203 rved treatment effects seemed independent of FGFR2 mutation status.

204 Activating FGFR2 mutations are found in 10-16% of primary endometri

205 We have identified de novo FGFR2 mutations in a sporadically occurring perinatal le

206 Inhibition of p53 in cells expressing the FGFR2 mutations in BBDS rescues delayed osteoblast diffe

207 We previously showed that FGFR2 mutations in BBDS, which amplify nucleolar targeti

208 By studying dominant FGFR2 mutations that are germline in bent bone dysplasia

209 Previously, we showed that the unique FGFR2 mutations that cause BBDS reduce receptor levels a

210 sorders, including Apert syndrome (caused by FGFR2 mutations), achondroplasia, and thanatophoric dysp

211 and was more than 100-fold selective against FGFR2-negative cell lines.

212 Second-line dovitinib in FGFR2(mut) and FGFR2(non-mut) advanced or metastatic endometrial cancer

213 to be treatment-related: one patient in the FGFR2(non-mut) group died from cardiac arrest with contr

214 ut) group and nine (29.0%, 14.2-48.0) in the FGFR2(non-mut) group were progression-free at 18 weeks.

215 the FGFR2(mut) group and 31 patients in the FGFR2(non-mut) group.

216 cancer and in those with FGFR2-non-mutated (FGFR2(non-mut)) endometrial cancer.

217 2(mut)) endometrial cancer and in those with FGFR2-non-mutated (FGFR2(non-mut)) endometrial cancer.

218 Moreover, Fgfr2 null epithelium was unable to undergo ductal branc

219 to class I with the minor alleles of SNPs in FGFR2 (odds ratio [OR] = 2.1, P = 0.004) and declined wi

220 elium, and downregulation of FGF receptor 2 (FGFR2) on PMNs rescued host defense in these mice.

221 urothelial and endometrial cancer (all with FGFR2 or FGFR3 translocations); 16 patients had stable d

222 Deletion of Fgfr2 or its ligand Fgf10 results in severe hypospadias

223 I risk increased versus class I with SNPs in FGFR2 (OR 2.2, P = 0.005) and COL1A1 (OR = 2.1, P = 0.00

224 lls, in which any one of three FGFRs (FGFR1, FGFR2, or FGFR3) is sufficient for survival.

225 ne novel locus associated with TG near WDR11-FGFR2 (P = 2.7 x 10-10).

226 Concurrently, Shp2 cycles between its FGFR2-phosphorylated and dephosphorylated forms.

227 Upon stimulation, FGFR2 phosphorylates tyrosine residues on Grb2, promotin

228 this background cycling, promoting increased FGFR2 phosphorylation and kinase activity, Grb2 dissocia

229 trate that differential expression levels of FGFR2, Plcgamma1 and Grb2 correlate with patient surviva

230 tro Pharmacokinetic analyses in mice bearing FGFR2-positive NCI-H716 tumors indicated that the toxoph

231 ng analyses, we report a novel fusion event, FGFR2-PPHLN1 (16%), and damaging mutations in the ARAF o

232 l translocation t(10;12)(q26;q12) leading to FGFR2-PPHLN1 fusion possesses transforming and oncogenic

233 impairs its ability to bind to its substrate FGFR2 pre-mRNA.

234 Of 248 patients with FGFR2 prescreening results, 27 (11%) had FGFR2(mut) endo

235 Fibroblast growth factor receptor 2 (FGFR2) promotes osteoprogenitor proliferation and differ

236 l, a single HS chain interacts with the FGF2-FGFR2 protein complex through a single S-domain that can

237 c canyon located on the top face of the FGF2-FGFR2 protein complex.

238 hains are proposed to interact with the FGF2-FGFR2 protein complex.

239 otspots in the tyrosine kinase domain of the FGFR2 protein, one of which is also a hotspot in breast

240 lates cell cycle exit via components of FGF (Fgfr2, Prox1 and Ccnd1) and Wnt (Dkk3, Wnt7a, Lrp6, Bcl9

241 FGFR2 rather selectively repressed the Nanog gene with m

242 Using model systems we show that FGFR2-regulated genes are preferentially linked to breas

243 Here, we show that Fgfr2 regulates both the formation and resolution of tet

244 al anomalies, cellular analysis reveals that Fgfr2 regulates epithelial maturation and cell cycle pro

245 se features we would suggest represent a new FGFR2-related syndrome, craniosynostosis with XY male-to

246 thral epithelium, whereas loss of ectodermal Fgfr2 results in severe hypospadias and absence of the v

247 expected finding that ectodermal deletion of Fgfr2 results in the most severe hypospadias highlights

248 Conditional deletion of Fgfr2 results in two distinct phenotypes: endodermal Fgf

249 , we reveal a mechanistic connection between FGFR2, ribosome biogenesis, and cellular stress that lin

250 ocus is consistent with the finding that the FGFR2 risk locus primarily predisposes to estrogen-recep

251 d were with imputed SNPs residing within the FGFR2 (rs1219515, P = 1.1 x 10(-5)) and PAPSS2 (rs196982

252 iduals who carried the polymorphic allele of FGFR2 (rs1219648) presented higher risk for having premo

253 68277 (CASP8), rs1982073 (TGFB1), rs2981582 (FGFR2), rs13281615 (8q24), rs3817198 (LSP1), rs889312 (M

254 Mice with point mutations in Fgfr2's binding site for the docking protein Frs2alpha (

255 receptor, resulting in up-regulation of both FGFR2's kinase and Shp2's phosphatase activity.

256 ation we simultaneously induce expression of Fgfr2(S252W) and beta-galactosidase in either the neural

257 ovel mechanism of suture fusion in the Apert Fgfr2(S252W) mouse model.

258 unanticipated role for p63-driven paracrine FGFR2 signaling as an addicting pathway in human cancer

259 ormation and suggests that the miR-327-FGF10-FGFR2 signaling axis may be a therapeutic targets for tr

260 netic contexts, maintaining normal levels of FGFR2 signaling is important for human testis determinat

261 Contrary to in vitro findings, Fgfr1 and Fgfr2 signaling is not required for the proliferation of

262 a feedback loop induced by MEK inhibition on FGFR2 signaling pathway.

263 mor-survival program involving p63-regulated FGFR2 signaling that was activated by ligand emanating f

264 tween two developmental pathways affected by FGFR2 signaling, possibly offering a junction to exploit

265 phenotype that can be reverted by inhibiting FGFR2 signaling.

266 ontrols fibroblast growth factor receptor 2 (FGFR2) signaling by regulating receptor kinase and SH2 d

267 We show that FGFR2 signalling correlates with maintenance of expressi

268 uggesting that ERK1/2 are key transducers of FGFR2 signals for myelin growth.

269 Analysis of the FGFR2-skeletal disorder bent bone dysplasia syndrome (BB

270 r2 was efficiently deleted in this tissue in Fgfr2(ST-/-) mice at embryonic day (E) 10.5.

271 le ureters were histologically normal, E15.5 Fgfr2(ST-/-) mice exhibit improper ureteral insertion si

272 E10.5 Fgfr2(ST-/-) mice had decreases in Bmp4 mRNA in stromal

273 E11.5 Fgfr2(ST-/-) mice had randomized UB induction sites with

274 We conditionally deleted Fgfr2 in ST (Fgfr2(ST-/-)) using Tbx18cre mice.

275 sed signaling models, the symmetric FGF2-HS2-FGFR2 ternary complex model and the asymmetric FGF2-HS1-

276 port a preference for the symmetric FGF2-HS2-FGFR2 ternary complex model.

277 ry complex model and the asymmetric FGF2-HS1-FGFR2 ternary complex model.

278 on was able to interact with the promoter of FGFR2, the likely target gene of this risk region.

279 at the BBDS mutations augment the ability of FGFR2 to recruit histone-remodeling factors that epigene

280 the alternative splicing of FGF receptor-2 (FGFR2) transcripts, altering the incorporation of casset

281 nstrate fibroblast growth factor receptor 2 (FGFR2) triggers Nanog gene down-regulation and different

282 histological assessment showed that, whereas Fgfr2(UB-/-) kidneys had more severe ureteric branching

283 ric branching defects than Frs2alpha(UB-/-), Fgfr2(UB-/-) kidneys were indistinguishable from Fgfr2/F

284 -/)) were compared with Frs2alpha(UB-/-) and Fgfr2(UB-/-) mice.

285 neys were more severely affected than either Fgfr2(UB-/-) or Frs2alpha(UB-/-) kidneys.

286 irmed that Fgfr2 is expressed in ST and that Fgfr2 was efficiently deleted in this tissue in Fgfr2(ST

287 n the dentate gyrus were deficient even when FGFR2 was lacking only in adulthood.

288 FGF4 ligand and FGFR2 were detected primarily on the plasma membrane of

289 s, and 14 markers in AXIN2, FGF3, FGF10, and FGFR2 were genotyped.

290 ences in allele specific expression (ASE) of FGFR2 were not observed in a panel of 72 ERalpha positiv

291 for this transcriptional down-regulation by FGFR2, when the reporter transgenes were integrated with

292 t observed by LM-PCR (Myc, Akt1, Pth, Csf1r, Fgfr2, Wisp1, Map3k5, and Map4k3).

293 tly, it provides compelling evidence linking FGFR2 with the ERK1/2-MAPK pathway, which converges with

294 associations between AXIN2, FGF3, FGF10, and FGFR2 with tooth agenesis [i.e., individuals who carried

295 unique and additive activities of FGFR1 and FGFR2 within the ICM coordinate establishment of two dis

296 XY Fgf9/Wnt4 and Fgfr2/Wnt4 double mutants developed testes with male som

297 e developed a mouse model of BSS harboring a FGFR2 Y394C mutation and identified p38 MAPK as an impor

298 study reveals the pleiotropic effects of the FGFR2 Y394C mutation evidenced by cutis gyrata, acanthos

299 Fgfr2+/Y394C mice exhibited epidermal hyperplasia and pr

300 Treating Fgfr2+/Y394C mice with a p38 kinase inhibitor attenuated

301 cally, they show how alternative splicing of FGFR2 yields heteroisoforms critical to the growth-promo