ライフサイエンスコーパス: FGFR1

1 FGFR1 affects brain cell development by two distinct mec

2 FGFR1 gene expression regulates myoblast proliferation a

3 FGFR1 in the kidney may provide a new molecular target f

4 FGFR1 is a principal cause for these less severe disease

5 FGFR1 isoforms are formed from alternate splicing of exo

6 FGFR1 silencing also reduced expression of HIF1alpha, wh

7 FGFR1 with the duplication induced FGFR1 autophosphoryla

8 FGFR1, FGF2, and FGF18 were overexpressed in mesotheliom

9 nts in Fibroblast Growth Factor Receptor 1 ( FGFR1) and report a novel, de novo variant in FGFR1 in a

10 licated fibroblast growth factor receptor 1 (FGFR1) and canonical WNT/beta-catenin signaling in prost

11 e fibroblast growth factor (FGF) receptor 1 (FGFR1) are a feature of stem cell leukemia-lymphoma synd

12 Here we examined FGF receptor 1 (FGFR1) expression and investigated its in vivo function

13 EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis.

14 The fibroblast growth factor receptor 1 (FGFR1) is ectopically expressed in prostate carcinoma ce

15 tion of fibroblast growth factor receptor 1 (FGFR1) or pretreatment with inhibitors of mitogen-activa

16 Fibroblastic growth factor receptor 1 (FGFR1) signaling pathways are implicated in the regulati

17 A), and fibroblast growth factor receptor 1 (FGFR1) to cell proliferation and apoptosis via the PIM a

18 such as fibroblast growth factor receptor 1 (FGFR1), concomitant inhibition of FGFR1 and MET blocked

19 alysis, fibroblast growth factor receptor 1 (FGFR1)-5-hydroxytryptamine 1A (5-HT1A) receptor complexe

20 pathway after binding to the FGF receptor 1 (FGFR1).

21 cluding fibroblast growth factor receptor 1 (FGFR1).

22 clude FGFs via activation of FGF receptor 1 (FGFR1).

23 s fibroblast growth factor (FGF) receptor-1 (FGFR1) independent of FGF ligand in liver endothelial ce

24 K7) and fibroblast growth factor receptor-1 (FGFR1), which are thought to be specific to post-implant

25 receptor-type, but not FGF receptor type 1 (FGFR1), resulted in attenuation of myelin growth, expres

26 Fibroblast Growth Factor receptors-1 and -2 (FGFR1/2) in oligodendrocytes also resulted in downregula

27 e for the therapeutic targeting of the FGF-2/FGFR1/CEP57 axis in prostate cancer.

28 ) of fibroblast growth factor receptors 1-3 (FGFR1 to -3) generates epithelial FGFR1b-FGFR3b and mese

29 the 5-HT1A autoreceptors by being part of a FGFR1-5-HT1A receptor heterocomplex in the midbrain raph

30 selectively interact in vivo with activated FGFR1.

31 cell lymphoma cells (LCs) through activating FGFR1 upregulates the Notch ligand Jagged1 (Jag1) on nei

32 Ablation of adipose FGFR1 resulted in increased hepatosteatosis under starva

33 ters are necessary for mediating most or all FGFR1 signaling, not only in MGE differentiation, but al

34 he NPT2A phosphate transporter, alphaKlotho, FGFR1, FGFR3, FGFR4, and the PTH receptor.

35 reduced 6-O-sulfation is preserved, although FGFR1 activation is inhibited correlating with reduced r

36 An FGFR1-SPRY2 signaling axis has previously been character

37 ated the anti-cancer benefits of AZD4547, an FGFR1-3 inhibitor, in ErbB2-overexpressing breast cancer

38 Furthermore, cKL stimulated Fgf23 in an FGFR1-dependent manner in bone cells.

39 ng TM domains from other receptors, EGFR and FGFR1, failed to stimulate TrkB phosphorylation.

40 and miR-503, which directly target FGF2 and FGFR1.

41 rom ASMCs to T cells was partially FGF2b and FGFR1 dependent.

42 nct from the reduced expression of IGF2R and FGFR1.

43 Overall, these data suggest that KLB and FGFR1 form a 1:1 heterocomplex independent of the galect

44 Differential regulation of renal Klotho and FGFR1 in normal and uremic rats.

45 epancy between FGFR1 amplification level and FGFR1 protein expression in a number of these cell lines

46 with increased mitochondrial metabolism and FGFR1 signaling.

47 identified orphan nuclear receptor Nurr1 and FGFR1 as essential factors in development of mesencephal

48 ly active population and that both Nurr1 and FGFR1 bind to a common region in the TH gene promoter.

49 experiments showed the presence of Nurr1 and FGFR1 in common nuclear protein complexes.

50 tically exploited by targeting the PDGFR and FGFR1 pathways to block relapse and metastasis of advanc

51 lecular lesions BCR/ABL, PDGFRA, PDGFRB, and FGFR1.

52 0, also regulates myoblast proliferation and FGFR1 promoter activity.

53 roblasts caused an increase in Fgfr1 RNA and FGFR1 protein expression levels that resulted in increas

54 Blocking FGF2b's synthesis and FGFR1 function reduced LMC formation.

55 sensitive to combined endocrine therapy and FGFR1 inhibition.

56 VEGFR2 and FGFR1 activation in PCECs therefore increases MMP14-depe

57 c activation of FGFR1 with a monoclonal anti-FGFR1 antibody (R1MAb1) normalized BP and significantly

58 Instead, autocrine FGFR1 and PDGFRalpha signaling, which have not been prev

59 ated with lymph-node metastases (INHBB, AXL, FGFR1, and PDFGRB) and upregulation of INHBB and AXL in

60 report that there was a discrepancy between FGFR1 amplification level and FGFR1 protein expression i

61 ited by dose-limiting toxicities mediated by FGFR1-3 receptors.

62 t is likely receptor mediated, albeit not by FGFR1, FGFR2, and FGFR3.

63 pathogenic cysteine substitutions: the C178S FGFR1 mutant, the C342R FGFR2 mutant, and the C228R FGFR

64 In pancreatic islet beta-cells, canonical FGFR1 signaling affects metabolism and insulin processin

65 2 and KEAP1 mutations, PI3K pathway changes, FGFR1 amplification, and DDR2 mutations.

66 model of transcriptional control of chicken FGFR1 gene regulation during myogenesis is presented.

67 imary human disease, demonstrated that CNTRL-FGFR1, through abnormal activation of several signaling

68 expression of the FGF21 receptor components, FGFR1 and betaKL, and also that of SIRT1, resulting in F

69 jection and bile duct ligation, constitutive FGFR1 signalling in liver sinusoidal endothelial cells c

70 pic analogies between mice with constitutive FGFR1 activation and Nf1 deficiency in Col2a1-positive c

71 In contrast, FGFR1-amplified high FGFR1 protein-expressing lung cance

72 whether neurofibromin is required to control FGFR1-Ras-ERK signaling in maturing chondrocytes in vivo

73 ases with targetable mutations in SMO, DDR2, FGFR1, PTCH1, FGFR2, and MET Our results indicate that a

74 erestingly, in one HPE family, a deleterious FGFR1 allele was transmitted from one parent and a loss-

75 on of both membrane FGFRs and INFS-dependent FGFR1 pathways may provide a means to integrate systemic

76 ctivate other kinases, including BLNK, DGKH, FGFR1, IL2RB, LYN, NTRK3, PDGFRA, PTK2B, TYK2, and the R

77 nditional knockout (cKO) of FGFR1 in the DT (FGFR1(DT-cKO) mice) resulted in left ventricular hypertr

78 e recorded the phenotype resulting from each FGFR1 variant to generate a series of phenotype-specific

79 st a critical and permissive role of ectopic FGFR1 signaling in prostate tumorigenesis and particular

80 We identified EFNB2, FGFR1, FGFR2, INSR, IRS2, NOTCH2, TLE1, and NTRK2 as nov

81 luding alterations in ALK, ARAF, BRAF, EGFR, FGFR1, FGFR2, KIT, KRAS, MAP2K1, MET, NF1, NF2, NRAS, RA

82 genes, we detected mutations in ERBB2, EGFR, FGFR1, PDGFRA, and MAP2K1 as potential mechanisms of pri

83 ditional growth factor receptor genes (EGFR, FGFR1, IGF1R, LIFR, and NGFR) also showed recurrent gain

84 strongly correlated with loss of endothelial FGFR1 expression, activation of endothelial TGF-beta sig

85 oscillatory shear stress reduced endothelial FGFR1 expression and activated TGF-beta signaling.

86 NB2, AR, ADCY1, DNMT3B, SMAD2, AMHR2, ERBB2, FGFR1, MAP3K12 and THEM4 were specifically selected in t

87 peutically targetable kinases such as ERBB2, FGFR1, FGFR2, EGFR, and MET, suggesting the potential us

88 TbetaRIII bound FGF2 and exogenous FGFR1, which promoted neuronal differentiation of neurob

89 ly active in BaF3 cells expressing exogenous FGFR1 chimeric kinases cultured in vitro as well as in T

90 of Trp53-null neonatal astrocytes expressing FGFR1 with the duplication involving the TKD into the br

91 TSCs to express FGF4, inducing a feedforward FGFR1-ETS2 angiocrine cascade that obviates TEC IGFBP7.

92 with increased hepatic expression of FGF10, FGFR1, and FGFR2 as well as mesenchymal genes SLUG and S

93 ify MEKK4 as a critical hub kinase for FGF20-FGFR1 signaling to induce HC differentiation in the mamm

94 4 acts as a critical node to integrate FGF20-FGFR1 signaling responses to specifically influence HC d

95 nse of FGFR1 during HC development and FGF20/FGFR1 signaling activated MEKK4 for normal sensory cell

96 first demonstrated the expression of FGF21, FGFR1 and FGFR3 (two receptors known to be activated by

97 Thus, targeting the angiocrine FGF4-FGFR1/Jag1-Notch2 loop inhibits LC aggressiveness and en

98 and upregulation of IGF1 activates the FGF4-FGFR1-ETS2 pathway in TECs and converts naive tumor cell

99 showed reduced expression of FGF10, FGFBP3, FGFR1, FGFR2b, and FGFR3, major local drivers of angioge

100 lso demonstrated in human SCLL- and FGFR1OP2-FGFR1-expressing KG-1 cells.

101 rsor cells, in which any one of three FGFRs (FGFR1, FGFR2, or FGFR3) is sufficient for survival.

102 o-regenerative CXCR7-Id1 versus pro-fibrotic FGFR1-CXCR4 angiocrine pathways in vascular niche balanc

103 Finally, FGFR1 silencing delayed the growth of irradiated tumor x

104 We find FGFR1-PLAG1 in seven (18%) cases, and the novel TGFBR3-P

105 653/654 and 766 residues are required for FN-FGFR1 activation of AKT and chemotaxis.

106 FOP (FGFR1 Oncogene Partner) is a known centrosome protein wi

107 FOP-FGFR1, an oncogenic fusion that causes a form of leukemi

108 Localization of the FOP-FGFR1 fusion kinase to centriolar satellites may be rele

109 We identify target genes for FGFR1, which exert significant effects on cell migration

110 a downstream effector signaling molecule for FGFR1, was sufficient to produce similar effects, arguin

111 The homo-interaction signal observed for FGFR1 was indeed as robust as that obtained for epiderma

112 ossibility, we evaluated a specific role for FGFR1 in glioblastoma radioresistance as modeled by U87

113 and uncover novel therapeutic strategies for FGFR1-amplified SCC with low FGFR1 protein expression.

114 est that clinical efficacy of treatments for FGFR1-driven lung cancers and HNSCC may be achieved by c

115 ta reveal that biomarker-directed trials for FGFR1-amplified SCC require assessment of FGFR1 protein

116 Notably, tumor xenografts generated from FGFR1-dependent lung cancer cells exhibited only modest

117 In vitro studies showed that FGFR1 G260E, FGFR1 R756H, and PROKR2 R85H are loss-of-function mutati

118 the fibroblast growth factor receptor 1 gene FGFR1 (G260E and R756H), two in the prokineticin recepto

119 roblast growth factor receptor (FGFR) genes (FGFR1 or FGFR3) to the transforming acidic coiled-coil (

120 clude seven of nine Src family kinase genes, FGFR1, FGFR2, ITK, NTRK1, NTRK2, MOS, MST1R, and RAF1.

121 In contrast, FGFR1-amplified high FGFR1 protein-expressing lung cancers are sensitive to F

122 ve for the fgfr1 null allele, exhibited high FGFR1 expression, and a neuroendocrine phenotype regardl

123 Addition of a PI3K inhibitor to these high FGFR1 protein-expressing cancers further sensitized them

124 5-HT1A receptor protomer in the hippocampal FGFR1-5-HT1A receptor complex enhancing the FGFR1 signal

125 ior in FGF receptor (FGFR) KO mice; however, FGFR1, FGFR2, and FGFR3 KO mice did not mimic the phenot

126 ole for the inflammatory chemokine CX3CL1 in FGFR1-induced macrophage migration.

127 atures that appear to govern the DFG flip in FGFR1.

128 tion of Klotho expression and an increase in FGFR1.

129 l with a c.1638C>A (p.Asn546Lys) mutation in FGFR1.

130 Mutations in FGFR1 have recently been associated with Hartsfield synd

131 es are the most commonly mutated residues in FGFR1 in human cancers and are associated primarily with

132 ess FGF-23, but did not induce a response in FGFR1(DT-cKO) mice.

133 GFR1) and report a novel, de novo variant in FGFR1 in an individual with multiple congenital anomalie

134 general and diseases caused by variation in FGFR1 specifically.

135 composed of FGF receptors (FGFRs), including FGFR1, and alpha-Klotho in the kidney distal tubule (DT)

136 a result, 12 hits were identified including FGFR1 (FGF receptor 1), TrkB, and TrkC as well as compon

137 of the activation loop, with some, including FGFR1 kinase, appearing refractory to this so-called 'DF

138 r activity in several tumor types, including FGFR1-amplified sqNSCLC and FGFR3-mutant bladder/urothel

139 In summary, high FGF23 levels increase FGFR1, whereas phosphaturia decreases Klotho expression

140 -HT1A agonist also synergistically increased FGFR1 and ERK1/2 phosphorylation in the raphe midline ar

141 lular domain, mediate the ligand-independent FGFR1 dimerization.

142 FGFR1 with the duplication induced FGFR1 autophosphorylation and upregulation of the MAPK/E

143 Subsequent addition of FGF21 induced FGFR1 dimerization without changing KLB aggregate size,

144 honous transgenic mouse models for inducible FGFR1 (JOCK1) and prostate-specific and ubiquitously exp

145 dies have shown that activation of inducible FGFR1 (iFGFR1) in mammary epithelial cells resulted in i

146 strate that activation of both the inducible FGFR1 construct in mouse mammary epithelial cells and en

147 cell membrane protein beta-Klotho, inducing FGFR1 phosphorylation.

148 RNAi to determine the effects of inhibiting FGFR1 or FGFR3 in a panel of human BC cell lines.

149 cell surface FGF receptors and intranuclear FGFR1, to determine the roles of membrane FGFRs and inte

150 Several cell models were used to investigate FGFR1 inhibition in vitro and in combination with cispla

151 the PrE-specific expression of FGFR2, it is FGFR1, expressed by all ICM cells, that is critical for

152 mediated by paracrine FGF control of kidney FGFR1 and subsequent regulation of soluble Klotho and TR

153 s167, and the human receptor tyrosine kinase FGFR1 and cardiac IKS potassium channel.

154 that the oncogenic receptor tyrosine kinase FGFR1 directly phosphorylates LDH-A.

155 However, 6 d later, FGFR1/2/3 loss of function reduced dendritic branch numb

156 cells to monitor dimerization of full-length FGFR1 at the cell-surface with or without the coreceptor

157 OFCC1/TFAP2A, TAF1B, FGF10, MSX1, LINC00640, FGFR1 and SPRY1).

158 lines, and the cancers with unexpectedly low FGFR1 expression were uniformly resistant to the differe

159 strategies for FGFR1-amplified SCC with low FGFR1 protein expression.

160 moter activity in myoblasts and Sp1-mediated FGFR1 promoter activity in Drosophila SL2 cells.

161 h contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual p

162 utations, HER2 insertions, PIK3CA mutations, FGFR1 amplifications, DDR2 mutations, ROS1 rearrangement

163 nd/or chemotactic in vivo, dominant negative FGFR1 was electroporated into the premigratory cardiac n

164 ific kinase inhibitor or a dominant-negative FGFR1 construct led to significantly decreased prolifera

165 or by transfection with a dominant-negative FGFR1 construct.

166 Here we demonstrate that of the nine FGFR1 mutations recently detected in our screen of over

167 increase of mDA neurons and enhanced nuclear FGFR1 accumulation.

168 Furthermore, nuclear FGFR1 or its 23-kDa FGF-2 ligand (FGF-2(23)) enhances Nu

169 es of membrane FGFRs and integrative nuclear FGFR1 signaling (INFS) in the regulation of FGF-23 gene

170 or cells, whereas direct integrative nuclear FGFR1 signaling (INFS) is associated with an exit from t

171 nstrated the Nurr1-mediated shift of nuclear FGFR1-EGFP mobility toward a transcriptionally active po

172 Here, we show that nuclear FGFR1 and Nurr1 are expressed in the nuclei of developin

173 ribe WNT-induced synergistic acceleration of FGFR1-driven adenocarcinoma, associated with a pronounce

174 F2 promoted resistance through activation of FGFR1 and downstream MAPK effectors; these resistant cel

175 o increased IL-8 secretion via activation of FGFR1 and Smad 3 signaling.

176 FN activation of FGFR1 requires beta1 integrin, as evidenced by neutraliz

177 Pharmacologic activation of FGFR1 with a monoclonal anti-FGFR1 antibody (R1MAb1) nor

178 el whereby unique and additive activities of FGFR1 and FGFR2 within the ICM coordinate establishment

179 or FGFR1-amplified SCC require assessment of FGFR1 protein expression and uncover novel therapeutic s

180 eoblasts through a cAMP-dependent binding of FGFR1 and cAMP-response element-binding protein (CREB) t

181 Conditional knockout (cKO) of FGFR1 in the DT (FGFR1(DT-cKO) mice) resulted in left ve

182 Transcriptional cooperation of FGFR1 with Nurr1 was confirmed on isolated Nurr1-binding

183 at Flk1-Cre or Tie2-Cre mediated deletion of FGFR1 and FGFR2 (Fgfr1/2(Flk1-Cre) or Fgfr1/2(Tie2-Cre)

184 FGF22 deficiency or the targeted deletion of FGFR1 and FGFR2 in the hindlimb motor cortex limits the

185 656Glu) within the tyrosine kinase domain of FGFR1, in two affected individuals each.

186 that Ser(779) in the cytoplasmic domains of FGFR1 and FGFR2 is required for the sustained activation

187 We identify a novel pathway downstream of FGFR1 activation, whereby the receptor is cleaved and tr

188 n raphe cells, evidence for the existence of FGFR1-5-HT1A receptor heterocomplexes in the dorsal and

189 r, mRNA expression and protein expression of FGFR1 were assessed in cell lines, tumor specimens and d

190 Expression of FGFR1, -2, and -4 was identified in human CCA cell lines

191 , and were correlated with the expression of FGFR1.

192 The hearts of FGFR1(DT-cKO) mice showed increased expression of the tr

193 nergistically to combinatorial inhibition of FGFR1 and FLT3.

194 Accordingly, co-inhibition of FGFR1 and HER2 or PDGFRalpha led to enhanced drug respon

195 eceptor 1 (FGFR1), concomitant inhibition of FGFR1 and MET blocked this compensatory HGF upregulation

196 In contrast, inhibition of FGFR1 by a specific kinase inhibitor or a dominant-negat

197 Pharmacological inhibition of FGFR1 signalling blocked MAPK activation and colony grow

198 Inhibition of FGFR1 synergistically enhanced the cytotoxic effects of

199 evelop an irreversible covalent inhibitor of FGFR1-4 for use in oncology indications.

200 mour cell responses to two new inhibitors of FGFR1-3, AZ12908010 and the clinical candidate AZD4547,

201 ependent complex by the c-spliced isoform of FGFR1 and betaKlotho.

202 High levels of FGFR1 protein and activated pFRS2alpha signalling were o

203 ecognizes a site in the upper kinase lobe of FGFR1 that is revealed by displacement of the kinase dom

204 pendent of either hematopoietic cell loss of FGFR1/2 or vascular endothelial growth factor receptor 2

205 recruit Src kinase, an important mediator of FGFR1 signaling, as a result of the translocations that

206 ng that PLCgamma is an essential mediator of FGFR1-induced radioresistance.

207 ociated variants to a 3-dimensional model of FGFR1 to assess which protein domains harbored the highe

208 a 5-HT1A agonist induced phosphorylation of FGFR1 and extracellular signal-regulated kinase 1/2 in r

209 activates ERK, FN-induced phosphorylation of FGFR1 preferentially activates AKT, indicating different

210 hereas FGF ligand-induced phosphorylation of FGFR1 preferentially activates ERK, FN-induced phosphory

211 Intragenic duplications of the portion of FGFR1 encoding the tyrosine kinase domain (TKD) and rear

212 how differential phosphorylation profiles of FGFR1 can achieve alternate downstream signals, and, mor

213 better understand the low response rates of FGFR1-amplified lung cancers to FGFR inhibitors, relatio

214 Transcriptional regulation of FGFR1 gene expression is developmentally regulated by th

215 Targeted resequencing of FGFR1 in multiple tissues from an independent cohort of

216 ation analysis of known tyrosine residues of FGFR1 reveals that tyrosine 653/654 and 766 residues are

217 ssion in regulating the specific response of FGFR1 during HC development and FGF20/FGFR1 signaling ac

218 However, the role of FGFR1 in regulating renal processes linked to hypertensi

219 ses controlling the intrinsic sensitivity of FGFR1-dependent lung cancer and head and neck squamous c

220 Sequencing of FGFR1 identified a previously unreported de novo variant

221 icating differential downstream signaling of FGFR1 in response to alternate stimuli.

222 ion in the non-phosphorylated basal state of FGFR1.

223 d phosphorylated FRS2, a direct substrate of FGFR1, as well as constitutive activation of RAS-MAPK si

224 se Src is required for FN transactivation of FGFR1.

225 mpting clinical investigations of the use of FGFR1 inhibitors for radiosensitization.

226 Orthotopic injection in vivo of FGFR1-silenced osteosarcoma cells caused a marked twofol

227 n of FGFRL1 as well as consequent effects on FGFR1 signaling and biological responses.

228 nd DDR2 gene mutations, ALK gene fusions, or FGFR1 gene amplifications.

229 -ABL1 or rearrangements of PDGFRA, PDGFRB or FGFR1.

230 ilia and rearrangement of PDGFRA, PDGFRB, or FGFR1, or with PCM1-JAK2" In addition to myeloproliferat

231 expression, attenuates pro-osteoclastogenic FGFR1 signaling in hypertrophic chondrocytes.

232 MTOR is an essential protein kinase in other FGFR1-expressing cancer cells.

233 The discovery of PDGFRA, PDGFRB, FGFR1, JAK-2, and FLT3 fusion proteins in patients with

234 34 (PRN1371), a highly selective and potent FGFR1-4 inhibitor.

235 d the pro-regenerative pathway and prevented FGFR1-mediated maladaptive subversion of angiocrine fact

236 n skeletal muscle in which pro-proliferative FGFR1 signaling is antagonized by SPRY1 to maintain sate

237 ew genetic alterations involving BRAF, RAF1, FGFR1, MYB, MYBL1 and genes with histone-related functio

238 ncreased expression of FGF2 and its receptor FGFR1 as a consequence of decreased expression of miR-42

239 last growth factor 2 (FGF2) and its receptor FGFR1, the malarial protein VAR2CSA, and tumor necrosis

240 inal relay neurons, while its main receptors FGFR1 and FGFR2 are expressed by cortical projection neu

241 FGF-10 and its receptors, FGFR1 and FGFR2, have been implicated in breast cancer s

242 een three fibroblast growth factor receptors-FGFR1, FGFR2, and FGFR3-in the absence of ligand.

243 KLF10 expression also significantly reduced FGFR1 promoter activity in myoblasts and Sp1-mediated FG

244 del to identify the mechanisms that regulate FGFR1-induced macrophage recruitment.

245 The data are consistent with regulated FGFR1 splicing involving a novel cytoplasmic mechanism.

246 23 enhanced phosphaturia and increased renal FGFR1 expression; however, Klotho expression was reduced

247 ssor of myoblast proliferation and represses FGFR1 promoter activity in these cells via an Sp1 bindin

248 KLF10 represses FGFR1 promoter activity and thereby myoblast proliferati

249 -bound structures have unexpectedly revealed FGFR1 for the first time in a 'DFG-out' state.

250 titumor activity of oral BGJ398, a selective FGFR1-3 tyrosine kinase inhibitor.

251 re, we investigated the effects of selective FGFR1 loss in the DT.

252 Silencing FGFR1 decreased radioresistance in a manner associated w

253 and show that blocking GrB activity stopped FGFR1 trafficking to the nucleus and abrogates the promi

254 Activation of cell surface FGFR1 by secreted FGFs stimulates proliferation of neura

255 ecifically influence HC development and that FGFR1 signaling through activation of MEKK4 is necessary

256 ts offer a preclinical proof of concept that FGFR1 targeting can degrade radioresistance in glioblast

257 Together, our data demonstrate that FGFR1 and FGFR3 have largely non-overlapping roles in re

258 development of the PrE and demonstrate that FGFR1 plays a more prominent role in this process than F

259 We observed that FGFR1 was expressed in BC cells that also expressed the

260 In vitro studies showed that FGFR1 G260E, FGFR1 R756H, and PROKR2 R85H are loss-of-fu

261 vivo relevance of our findings, showing that FGFR1 localized to the nucleus specifically in invading

262 integrity in the adult CNS and suggest that FGFR1/2 and Myrf may, in part, contribute to signaling u

263 It has been suggested that FGFR1 proteins lose their ability to recruit Src kinase,

264 The FGFR1 is a therapeutic target under investigation in mul

265 ant, Klotho expression remained low, and the FGFR1 level was reduced.

266 FGFR1-5-HT1A receptor complex enhancing the FGFR1 signaling.

267 is a critical mediator of signaling from the FGFR1 chimeric fusion genes generated by translocation i

268 coimmunoprecipitation and colocation of the FGFR1 and 5-HT1A immunoreactivities in the midbrain raph

269 o the proximal Sp factor binding site of the FGFR1 promoter and reduced Sp1 complex formation with th

270 Abnormal regulation of the FGFR1-Klotho receptor complex may cause a resistance to

271 Our findings establish the importance of the FGFR1-WNT-TGF-beta signaling axes as driving forces behi

272 yocardial protection by the mediation of the FGFR1/beta-Klotho-PI3K-Akt1-BAD signaling network.

273 ho is modulated by phosphaturia, whereas the FGFR1 expression is regulated by FGF23.

274 r and reduced Sp1 complex formation with the FGFR1 promoter at that site.

275 KLF10 interacts with the FGFR1 promoter, repressing its activity and cell prolife

276 Three FGFR1 mutations seen in HPE probands behave identical to

277 Signaling through FGFR1 is also required to constrain levels of the plurip

278 Thus, FGFR1 in the DT regulates systemic hemodynamic responses

279 post-translationally modified in response to FGFR1 signaling.

280 ral adipose tissue through the transmembrane FGFR1-KLB complex.

281 n HPE probands behave identical to wild-type FGFR1 in rescue assays, including one apparent de novo v

282 Although the existence of unliganded FGFR1 dimers on the surface of living cells has been pro

283 h we observed homodimerization of unliganded FGFR1 that is independent of its surface density.

284 vation mechanism and results in unrestrained FGFR1 ubiquitylation in cells.

285 Targeting growth factors using FGFR1 inhibitors may block survival pathways required by

286 SPGs promoted neuroblast differentiation via FGFR1 and ERK phosphorylation, leading to upregulation o

287 Whereas FGFR1-FGFR3 have been structurally characterized, the st

288 istone H3.1 p.Lys27Met substitution, whereas FGFR1 mutations or fusions occur in thalamic tumors asso

289 the existence of a signaling network wherein FGFR1-driven ERK and activated MTOR/AKT represent distin

290 R3 in prehypertrophic chondrocytes, and with FGFR1 in hypertrophic chondrocytes during endochondral o

291 yeloid and lymphoid neoplasm associated with FGFR1 is an aggressive disease, and resistant to all the

292 ryonic stem cell (ESC) differentiation, with FGFR1 again having a greater influence than FGFR2 in ESC

293 tes into the circulation and interacted with FGFR1 in cardiomyocytes under the mediation of the cell

294 ntly expanded the lung cancer landscape with FGFR1 amplification found in 10-20% of squamous cell car

295 In contrast, patients with FGFR1 and JAK2 fusion TK genes exhibit a more aggressive

296 ith BGJ398 doses >/= 100 mg in patients with FGFR1-amplified sqNSCLC and FGFR3-mutant bladder/urothel

297 During expansion at the MTD, patients with FGFR1-amplified squamous cell non-small-cell lung cancer

298 , has an overlapping expression pattern with FGFR1 and FGFR3 in prehypertrophic chondrocytes, and wit

299 In cells transfected with FGFR1 siRNA or ERK 1 siRNA, the antagonistic effects of

300 g prevented in chondrocytes transfected with FGFR1 siRNA or ERK1 siRNA.

301 phomas that arose in a murine model of ZMYM2-FGFR1 SCLL.