ライフサイエンスコーパス: FGFR1

1 FGFR1 gene expression regulates myoblast proliferation a

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

3 FGFR1 is a principal cause for these less severe disease

4 FGFR1 isoforms are formed from alternate splicing of exo

5 FGFR1 silencing also reduced expression of HIF1alpha, wh

6 FGFR1 stabilises N-cadherin at the cell membrane through

7 FGFR1, FGF2, and FGF18 were overexpressed in mesotheliom

8 FGFR1-3 gene expression was broadly distributed througho

9 FGFR1-amplified/ER+ breast cancer cells and MCF-7 cells

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

11 sion of fibroblast growth factor receptor 1 (FGFR1) and axonal guidance molecules known as neuropilin

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

13 ntified fibroblast growth factor receptor 1 (FGFR1) as the top target promoting survival of mesenchym

14 creased fibroblast growth factor receptor 1 (FGFR1) expression in NSCLC cell lines H1975, HCC827, and

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

16 ically, fibroblast growth factor receptor 1 (FGFR1) inhibition abolished the downstream signaling of

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

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

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

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

21 , EPHA2-fibroblast growth factor receptor 1 (FGFR1), EPHA2-FGFR2, EPHA2-FGFR3, VEGFR2-FGFR1, VEGFR2-F

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

23 cluding fibroblast growth factor receptor 1 (FGFR1).

24 ockade of the FGF2 receptor, FGF receptor-1 (FGFR1), suppresses alcohol consumption, and that the eff

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 the four FGF receptors (FGFRs 1-4), FGFR1 and FGFR3 are strongly implicated in osteoarthriti

29 ell regulator RORC in all three ASCPs, and a FGFR1-ERLIN2 fusion associated with focal CNVs in both g

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 actionable genes such as PIK3CA, EGFR, AKT3, FGFR1, ERBB2, ERBB3 and ESR1.

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

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

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 ar endothelial growth factor receptor 2) and FGFR1 (fibroblast growth factor receptor 1) after ischem

40 to BRAF V600E, AKT1 E17K, PIK3CA E542K, and FGFR1 or ERBB2 amplifications.

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

42 PCM with the cytoplasmic domains of EGFR and FGFR1.

43 protein kinase pathway genes (eg, ERBB2 and FGFR1) in 36% of the cases.

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

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

46 interactions between the endocrine FGFs and FGFR1/Klb, or FGF19 with FGFR4.

47 nct from the reduced expression of IGF2R and FGFR1.

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

49 KLOTHO and FGFR1 were also expressed in human germ cells and sperma

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

51 with increased mitochondrial metabolism and FGFR1 signaling.

52 e strongly implicated in osteoarthritis, and FGFR1 antagonists, as well as agonists of FGFR3, have sh

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

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

55 0, also regulates myoblast proliferation and FGFR1 promoter activity.

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

57 f HPE-associated genes ZIC2, GLI2, SMAD3 and FGFR1 in human neural stem cells.

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

59 ovalent targets of SM1-71 including TAK1 and FGFR1.

60 sensitive to combined endocrine therapy and FGFR1 inhibition.

61 The combination of EGFR TKI and FGFR1 or MEK inhibitors may offer an attractive therapeu

62 VEGFA, FGF2, and their receptors VEGFR2 and FGFR1, respectively, by directly binding to the compleme

63 Here we show that the bispecific anti-FGFR1/KLB agonist antibody BFKB8488A induced marked weig

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

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

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

67 s a critical event in the progression of BCR-FGFR1-driven leukemogenesis in stem cell leukemia and ly

68 ation of hematopoietic stem cells by the BCR-FGFR1 fusion kinase found in a variant of stem cell leuk

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

70 based gene fusion panel including ALK, BRAF, FGFR1, FGFR2, FGFR3, MET, NRG1, NTRK1, NTRK2, NTRK3, RET

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 The resultant Dr-EGFR and Dr-FGFR1 opto-RTKs are rapidly activated with near-infrared

86 ein-based biosensors enables simultaneous Dr-FGFR1 activation and detection of calcium transients.

87 FGF10-driven FGFR1 signaling is elevated in Rab23(-/-)sutures with a

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

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

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

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

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

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

94 ranscripts of growth factor receptors, EGFR, FGFR1, and FGRF2 than U cells.

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

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

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

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

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

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

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

102 We further show that the effects of FGF2-FGFR1 on alcohol drinking are mediated via activation of

103 ol consumption, and that the effects of FGF2-FGFR1 on alcohol drinking are mediated via the phosphoin

104 s and primary AML stroma; and increased FGF2/FGFR1 signaling is associated with increased exosome sec

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

106 4 acts as a critical node to integrate FGF20-FGFR1 signaling responses to specifically influence HC d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 Patients' tumors harbored FGFR1 or FGFR2 amplification (n = 20), FGFR2 or FGFR3 si

125 erved only in patients whose tumors harbored FGFR1-3 point mutations or fusions.

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

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

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

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

130 progression on CDK4/6 inhibitors identified FGFR1/2 amplification or activating mutations in 14/34 (

131 r ribociclib plus fulvestrant, we identified FGFR1 as a mechanism of drug resistance.

132 act cancer tumorigenesis include IDH1, IDH2, FGFR1, FGFR2, FGFR3, EPHA2, BAP1, ARID1B, ELF3, PBRM1, P

133 human CCA specimens by immunohistochemistry (FGFR1, 30% positive; and FGFR2, 65% positive) and the CC

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

135 tion of Klotho expression and an increase in FGFR1.

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

137 Mutations in FGFR1 have recently been associated with Hartsfield synd

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

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

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

141 general and diseases caused by variation in FGFR1 specifically.

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

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

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

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

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

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

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 prominent role of hypothalamic alpha-klotho/FGFR1/PI3K signaling in the modulation of NPY/AgRP neuro

155 king behavior via FGF receptor 1/Klothobeta (FGFR1/KLB) complexes expressed in adipocytes, pancreatic

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

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

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

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

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

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

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

163 Moreover, FGFR1 stimulates the anchoring of N-cadherin to actin.

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

165 sly unreported fusions identified were MYO5A-FGFR1, MYO5A-ERBB4, and PRKDC-CTNNB1.

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

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

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

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

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

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

172 Our results suggest that activation of FGFR1 by FGF2 in the DMS leads to activation of the PI3K

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

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

175 new biopsy at screening for the analysis of FGFR1-3 mRNA expression.

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

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

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

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

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

181 656Glu) within the tyrosine kinase domain of FGFR1, in two affected individuals each.

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

183 Upregulated expression of FGFR1 by hypoxia was mediated through the MAPK pathway a

184 um adiponectin and the adipose expression of FGFR1 target genes, demonstrating its action as an FGF21

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

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

187 , and were correlated with the expression of FGFR1.

188 to EGFR TKIs through increased expression of FGFR1.

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

190 Immunoprecipitation of FGFR1 coupled with mass spectroscopy indicated that FGFR

191 Importantly, inhibition of FGFR1 activity by a selective receptor antagonist reduce

192 nergistically to combinatorial inhibition of FGFR1 and FLT3.

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

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

195 Consistent with this, inhibition of FGFR1 function by the selective small-molecule inhibitor

196 alcohol consumption, and that inhibition of FGFR1 may provide a novel therapeutic target for alcohol

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

198 Inhibition of FGFR1 synergistically enhanced the cytotoxic effects of

199 ib is a selective, potent, oral inhibitor of FGFR1, 2, and 3.

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

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

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

203 H1975, HCC827, and YLR086, and knockdown of FGFR1 attenuated hypoxia-induced EGFR TKI resistance in

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

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

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

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

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

209 e to EGFR TKI is driven by overexpression of FGFR1 to sustain ERK signaling, where a subsequent combi

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

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

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

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

214 ib/fulvestrant induced complete responses of FGFR1-amplified/ER+ patient-derived-xenografts.

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

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

217 Sequencing of FGFR1 identified a previously unreported de novo variant

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

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

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

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

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

223 GFR3 single-nucleotide variants (n = 19), or FGFR1 or FGFR3 fusions (n = 9).

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

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

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

227 FGFR) 1-3 were treated with AZD4547, an oral FGFR1-3 inhibitor.

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

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

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

231 34 (PRN1371), a highly selective and potent FGFR1-4 inhibitor.

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

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

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

235 creases the expression of the FGF2 receptor, FGFR1 in the DMS.

236 Expression of FGF2 and its receptor, FGFR1, are both increased in a subset of stromal cell li

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

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

239 Recurrent FGFR1 variants in six patients, and ALK N-terminal struc

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

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

242 23 enhanced phosphaturia and increased renal FGFR1 expression; however, Klotho expression was reduced

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

244 KLF10 represses FGFR1 promoter activity and thereby myoblast proliferati

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

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

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

248 Silencing FGFR1 decreased radioresistance in a manner associated w

249 with similar binding affinity and stimulate FGFR1 activation and MAPK response.

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

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

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

253 oupled with mass spectroscopy indicated that FGFR1 forms a physical complex with NRPs, which is enhan

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

255 Confocal imaging revealed that FGFR1 and NRP1 predominantly interact throughout the cyt

256 Here we show that FGFR1 reduces N-cadherin-mediated cell migration.

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

258 The FGFR1 is a therapeutic target under investigation in mul

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

260 inhibitor against organoids derived from the FGFR1-ERLIN2 fusion-positive ASCP PDX model.

261 Importantly, systemic administration of the FGFR1 inhibitor PD173074 to mice, as well as its infusio

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

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

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

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

266 data suggest that specific activation of the FGFR1/KLB complex in humans can be used as therapy for o

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

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

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

270 Three FGFR1 mutations seen in HPE probands behave identical to

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

272 Thus, FGFR1 in the DT regulates systemic hemodynamic responses

273 post-translationally modified in response to FGFR1 signaling.

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

275 survival compared to patients with wild type FGFR1.

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

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

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

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

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

281 1 (FGFR1), EPHA2-FGFR2, EPHA2-FGFR3, VEGFR2-FGFR1, VEGFR2-FGFR2, and VEGFR2-FGFR3, using a FRET-base

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

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

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

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

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

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

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

289 th germ cells and spermatozoa and forms with FGFR1 a specific receptor for the bone-derived hormone F

290 ase receptor Tie2 physically interacted with FGFR1, promoting STAT3 phosphorylation and binding to th

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

292 ted throughout the CNS in Mus musculus, with FGFR1 exhibiting the greatest heterogeneity.

293 ial of ribociclib, showed that patients with FGFR1 amplification exhibited a shorter progression-free

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

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

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

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

298 re a subsequent combination of EGFR TKI with FGFR1 inhibitors or MEK inhibitors reverses this resista

299 cancer cells and MCF-7 cells transduced with FGFR1 were resistant to fulvestrant +/- ribociclib or pa

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