ライフサイエンスコーパス: FGFR3

1 eine in fibroblast growth factor receptor 3 (FGFR3).

2 ification of 18q21.3 (BCL2), 18q23, or 4p16 (FGFR3).

3 f human fibroblast growth factor receptor 3 (FGFR3).

4 tion in fibroblast-growth-factor-receptor 3 (FGFR3).

5 tion in fibroblast growth factor receptor 3 (FGFR3).

6 or mediated, albeit not by FGFR1, FGFR2, and FGFR3.

7 therapies target the extracellular domain of FGFR3.

8 prevents ligands from binding and activating FGFR3.

9 to skeletal pathology caused by mutations in FGFR3.

10 s of evidence suggest that proNodal acts via FGFR3.

11 ondroplasia disorders caused by mutations in FGFR3.

12 3, TRAF3, FAM46C, DIS3, BRAF, LTB, CYLD, and FGFR3.

13 R mutant resistant cancer with a mutation in FGFR3.

14 y enhancing tumor progression relative to WT FGFR3.

15 critical tyrosines in the activation loop of FGFR3.

16 an antagonistic relationship between UTX and FGFR3.

17 in skeletal diseases caused by mutations in FGFR3.

18 ral pre-messenger RNAs (pre-mRNAs) including FGFR3.

19 ase CHIP is able to interact and destabilize FGFR3.

20 FGFR3 and reduces the signaling capacity of FGFR3.

21 ween this construct and wild-type and mutant FGFR3.

22 regulated intramembrane proteolysis (RIP) of FGFR3.

23 ndividuals express both wild-type and mutant FGFR3.

24 osine (Y) 138 of HPV-31 E2 is a substrate of FGFR3.

25 t least in part the signaling from FGFR2 and FGFR3.

26 ng PIK3CA (2/13), STK11 (2/13), EGFR (1/13), FGFR3 (1/13), and PTPN11 (1/13).

27 Mfap5 mutation in the Fgfr3;4 mutant background partially attenuated the alveo

28 crofibril bridging factor, is upregulated in Fgfr3;4 mutants.

29 Here we show that in Fgfr3;Fgfr4 (Fgfr3;4) global mutant mice, alveolar simplification is

30 of the fibroblast growth factor receptor 3 (FGFR3), a receptor tyrosine kinase that negatively regul

31 e JM domain on unliganded dimer stability of FGFR3, a receptor that is critically important for skele

32 effect of two pathogenic point mutations in FGFR3 (A391E and G380R) on heterodimerization.

33 In microcultures, soluble FGFR3 abolishes Shh without affecting Gsc expression.

34 s further define the mechanisms that control FGFR3 accumulation and contribute to skeletal pathology

35 all molecule HDAC6 inhibitor tubacin reduced FGFR3 accumulation in the growth plate and improved endo

36 ylase HDAC6 (Histone Deacetylase 6) and that FGFR3 accumulation is compromised in cells lacking HDAC6

37 3 gene was replaced with human FGFR3(G380R) (FGFR3(ACH)) cDNA, the most common mutation in human ACH.

38 Heterozygous (FGFR3(ACH/+)) and homozygous (FGFR3(ACH/ACH)) mice expre

39 Heterozygous (FGFR3(ACH/+)) and homozygous (FGFR3(ACH/ACH)) mice expressing human FGFR3(G380R) recap

40 Similarly, NF449 antagonized FGFR3 action in the multiple myeloma cell lines OPM2 and

41 A homozygous deletions occur in a context of FGFR3-activating mutations, our model suggests that addi

42 We show that UTX loss and FGFR3 activation cooperate to disrupt the balance of lum

43 However, understanding of how FGFR3 activation drives urothelial malignant transformat

44 e investigate the effect of this mutation on FGFR3 activation in HEK 293 T cells over a wide range of

45 In contrast to UTX, FGFR3 activation was associated with lower expression of

46 egies for ACH, which aim to reduce excessive FGFR3 activation, have emerged over many years, the use

47 CL4 chemokines, both of which are induced by FGFR3 activation.

48 We have previously shown that mutant FGFR3 alters the cell-cell and cell-matrix adhesion prop

49 l mutation clusters in many proteins such as FGFR3 and CHRM2.

50 These are de novo missense variants in FGFR3 and COL2A1, and a de novo 16.8 kb deletion that in

51 xpression of KLF2, KLF4, VEGF-A, VEGF-C, and FGFR3 and elevated expression of p57.

52 Although Fgfr3 and Fgfr4 are expressed in the mesenchyme and epit

53 ic CRISPR-Cas9 approach, we demonstrate that fgfr3 and fgfr4 are required for vertebrate astrocyte mo

54 FGF signaling through receptors Fgfr3 and Fgfr4 is crucial for alveologenesis, but the m

55 were detected at activating positions in the FGFR3 and HRAS oncogenes.

56 Conversely, siRNA targeting FGFR3 and kdFGFR3 reduced clonogenicity, anchorage-indep

57 nduces the ubiquitination and degradation of FGFR3 and reduces the signaling capacity of FGFR3.

58 embers is sufficient to bypass dependency on FGFR3 and suggest that concurrent inhibition of these tw

59 ionship of Hsp90 and co-chaperone Cdc37 with FGFR3 and the FGFR family.

60 E mutations in dimerization of TM domains of FGFR3 and their consecutive contributions to the activat

61 r example, showing how mutual exclusivity of FGFR3 and TP53 mutations is interpretable if FGFR3 is mu

62 ions to fibroblast growth factor receptor 3 (FGFR3) and phosphatase and tensin homologue (PTEN) signa

63 tion of fibroblast growth factor receptor 3 (FGFR3) and PI3K/Akt signaling mechanisms leading to inhi

64 achondroplasia, and thanatophoric dysplasia (FGFR3), and Costello syndrome (HRAS), which we collectiv

65 amaging variants (UHMK1, AP1G2, DNTA, CHST6, FGFR3, and EPHA1) and 7 genes had associations with panc

66 splasias related to over-activation of human FGFR3, and for further studies of the underlying molecul

67 oteins cooperate to regulate VEGF-A, VEGF-C, FGFR3, and p57 by binding to the regulatory regions of t

68 endothelial growth factor (VEGF)-A, VEGF-C, FGFR3, and p57/CDKN1C genes.

69 ession of the spermatogonial markers MAGEA4, FGFR3, and phospho-AKT, whole genome amplification, and

70 Mutations in MYC, FGFR3, and VHL were identified for the first time.

71 FGFR3 antibodies have been associated with sensory neuro

72 and mutations that cause hyperactivation of FGFR3 are responsible for a collection of developmental

73 increased and/or inappropriate activation of FGFR3 are responsible for a collection of short-limbed c

74 he four FGF receptors (FGFRs 1-4), FGFR1 and FGFR3 are strongly implicated in osteoarthritis, and FGF

75 ions of fibroblast growth factor receptor 3 (FGFR3) are common in urothelial carcinoma of the bladder

76 Intriguingly, we have identified FGFR3 as a novel binding partner of PAK4 and observed si

77 Our results establish FGFR3 as a strong Hsp90 client and suggest that modulati

78 mediator of the oncogenic effects of mutant FGFR3, as its knockdown in FGFR3-mutant bladder cancer c

79 These results further our knowledge of FGFR3-associated bone disorders.

80 esults indicate that the KCNQ1OT1/miR-701-3p/FGFR3 axis is an important regulator of osteoblast proli

81 e-arrangements and a t(4;7) that generates a FGFR3-BAI1-associated protein 2-like 1 (BAIAP2L1) fusion

82 Fibroblast growth factor receptor 3 (FGFR3) belongs to a family of receptor tyrosine kinases

83 on 4p16.3, led to the loss of the 3'-UTR of FGFR3, blocking gene regulation of miR-99a and enhancing

84 atenin-deficient cochleae expressed FGF8 and FGFR3, both of which are essential for pillar cell speci

85 The active form of FGFR3 bound to and phosphorylated the region of amino ac

86 ilization of the unliganded dimeric state of FGFR3 by its JM and TM domains via a mechanism that is d

87 rential elimination of the dominant-negative FGFR3 c.1138G>A allele in fibroblasts of an individual a

88 main of fibroblast growth factor receptor 3 (FGFR3) causes achondroplasia, the most common form of hu

89 ProNodal and FGFR3 co-immunoprecipitate and proNodal increases FGFR3

90 Fibroblast growth factor receptor 3 (FGFR3) coimmunoprecipitated with the BPV-1 E2 protein, a

91 kinase fibroblast growth factor receptor 3 (FGFR3) complexes with and phosphorylates E2, which inhib

92 The FGFR3 component is identical in all cases and lacks the

93 er anti-fibroblast growth factor receptor 3 (FGFR3) compounds are showing promising results in the tr

94 dimers in cellular membranes, we designed an FGFR3 construct that lacks the kinase domain, and we mon

95 , our study reveals how mutations in UTX and FGFR3 converge to disrupt bladder differentiation progra

96 A constitutively active mutant form of FGFR3 decreased BPV-1 and HPV-31 transient replication a

97 ccumulation of FGFR3 was linked to increased FGFR3 degradation that occurred through a lysosome-depen

98 icient to drive resistance in the setting of FGFR3 dependency but not dependency on other FGFR family

99 ates TAZ as a possible therapeutic target in FGFR3-dependent bladder tumours.

100 two pathways may be desirable when targeting FGFR3-dependent cancers.

101 this model, UTX loss-of-function potentiated FGFR3-dependent transcriptional effects and the presence

102 Furthermore, FGFR3 depletion in cell lines that maintain HPV-31 episo

103 in emulates the action of fgf2, trapping the FGFR3 dimer in its most active state.

104 n and a TM pathogenic mutation on unliganded FGFR3 dimer stability are additive.

105 ons, Arg248Cys, Ser249Cys, and Tyr373Cys, on FGFR3 dimerization in mammalian membranes, in the absenc

106 It is believed that the mutation increases FGFR3 dimerization, and our results verify this.

107 /or lymphatic vascular defects seen in Fgfr1/Fgfr3 double mutant mice, while HK2 overexpression partl

108 C-type natriuretic peptide (CNP) antagonizes FGFR3 downstream signaling by inhibiting the pathway of

109 NVP-BGJ398 inhibited FGFR3 downstream signaling pathways, including MAPK, SOX

110 y SCD1 as a potential therapeutic target for FGFR3-driven bladder cancer.

111 ic nature of mutations observed in FGFR2 and FGFR3, each of which are observed in 3% of samples, for

112 ibroblast growth factor receptor 3-encoding (FGFR3-encoding) gene.

113 origenesis include IDH1, IDH2, FGFR1, FGFR2, FGFR3, EPHA2, BAP1, ARID1B, ELF3, PBRM1, PRKACA, PRKACB,

114 PLZF elevation increases FGFR3 expression and STAT3 pathway activity, suppresses

115 lated by exercise and cold in mice, and FGF9/FGFR3 expression in human neck fat is significantly asso

116 a T-cell depleted immune contexture; 3) High FGFR3 expression is enriched in UTUC and correlates with

117 Further, prechordal mesoderm cells in which Fgfr3 expression is reduced by Fgfr3 siRNA fail to bind

118 enchymal" markers ZEB1 and vimentin, whereas FGFR3 expression was restricted to the E-cadherin- and p

119 firmed or newly identified in PIK3CA, KMT2D, FGFR3, FBXW7, DDX3X, PTEN, TRAF3, RB1, CYLD, RIPK4, ZNF7

120 se, which expresses constitutively activated FGFR3 (FGFR3(K650E)) in postmitotic glutamatergic neuron

121 tiating a mutant activated knockin allele of FGFR3 (FGFR3K650E) that causes Thanatophoric Dysplasia T

122 A phosphate transporter, alphaKlotho, FGFR1, FGFR3, FGFR4, and the PTH receptor.

123 Here we show that in Fgfr3;Fgfr4 (Fgfr3;4) global mutant mice, alveolar simpl

124 ating with the FGFR1 inhibitor, SU5402 or an FGFR3 function-blocking antibody also slowed neural cres

125 le-nucleotide variants (n = 19), or FGFR1 or FGFR3 fusions (n = 9).

126 As urothelial cell lines with FGFR3 fusions are extremely sensitive to FGFR-selective

127 ous mouse Fgfr3 gene was replaced with human FGFR3(G380R) (FGFR3(ACH)) cDNA, the most common mutation

128 nial sutures and low bone density in newborn FGFR3(G380R) mice.

129 ygous (FGFR3(ACH/ACH)) mice expressing human FGFR3(G380R) recapitulate the phenotypes observed in ACH

130 corresponds to the copy number of activated FGFR3(G380R), and the phenotypes become more pronounced

131 hibition by exposure of cell lines harboring FGFR3 gene amplification and translocation to the select

132 CH mouse model in which the endogenous mouse Fgfr3 gene was replaced with human FGFR3(G380R) (FGFR3(A

133 istinct disorder caused by a mutation in the FGFR3 gene, featuring craniosynostosis, characteristic f

134 Collectively, our data suggest that FGFR3 GOF in postmitotic neurons not only alters axonal

135 cently, fibroblast growth factor receptor 3 (FGFR3) has also been reported to be a potential BoNT/A r

136 Whereas FGFR1-FGFR3 have been structurally characterized, the structur

137 ogether, our data demonstrate that FGFR1 and FGFR3 have largely non-overlapping roles in regulating i

138 nd FGFR1 antagonists, as well as agonists of FGFR3, have shown therapeutic efficacy in mouse models o

139 To investigate the formation of FGFR3 heterodimers in cellular membranes, we designed an

140 s form with lower probability than wild-type FGFR3 homodimers at low ligand concentration.

141 yrosine kinase inhibitor (TKI) to counteract FGFR3 hyperactivity has yet to be evaluated.

142 um of P0 cochlea lacking Jag1 Finally, using Fgfr3-iCreER(T2) ::Jag1(loxP/loxP) mice to delete Jag1 a

143 or abolishment of canonical Notch signaling (Fgfr3-iCreER; Rbpj(-/Delta)), indicating a critical role

144 d by small interfering RNA (siRNA; affecting FGFR3-IIIb and -IIIc) or an adenoviral kinase-dead FGFR3

145 Both FGFR3-IIIb and FGFR3-IIIc suppressed apoptotic activity,

146 Elevated levels of FGFR3-IIIb and/or -IIIc were found in 53% of HCC cases.

147 hepatoma/hepatocarcinoma cells, up-regulated FGFR3-IIIb conferred an enhanced capability for prolifer

148 FGFR3-IIIb overexpression occurred significantly more of

149 IIIb and -IIIc) or an adenoviral kinase-dead FGFR3-IIIc construct (kdFGFR3).

150 Both FGFR3-IIIb and FGFR3-IIIc suppressed apoptotic activity, enhanced clono

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

152 Silencing or inhibition of mutant FGFR3 in bladder cancer cell lines is associated with de

153 ally influence the stability and function of FGFR3 in disease.

154 led to increased expression and signaling of Fgfr3 in growth plate chondrocytes and suppression of ch

155 Sequencing of FGFR3 in KMS-11R cells revealed the presence of a hetero

156 verlapping expression pattern with FGFR1 and FGFR3 in prehypertrophic chondrocytes, and with FGFR1 in

157 ngs reveal a previously unrecognized role of FGFR3 in regulating lipid metabolism to maintain tumor g

158 a mechanism for the nuclear localization of FGFR3 in response to ligand activation, which may occur

159 examine the joint upregulation of WHSC1 and FGFR3 in samples with t(4;14)-related fusions, and we il

160 st growth factor receptors-FGFR1, FGFR2, and FGFR3-in the absence of ligand.

161 that wildtype and mutant activated forms of FGFR3 increase expression of the cytoplasmic deacetylase

162 Inhibition of FGFR3 increased target cell apoptosis through the suppre

163 anded our understanding of the mechanisms of FGFR3-induced disease and has increased the number of ap

164 ylalanine (F) mutant Y138F displayed reduced FGFR3-induced phosphotyrosine.

165 pertrophic chondrocytes, we show that mutant FGFR3 induces a differentiation block at this stage inde

166 A constitutive kinase-active FGFR3 inhibited wild-type (WT) E2-induced E1-dependent D

167 3 signaling with anti-Fgf23 antibodies or an FGFR3 inhibitor partially restored the suppression of Tn

168 In addition to FGFR3, integrin beta3 is another potential target for co

169 hat the fibroblast growth factor receptor 3 (FGFR3) interacts with and mediates PV E2 function throug

170 FGFR3 is expressed in proliferating chondrocytes of the

171 ithin the 3'-untranslated region (3'-UTR) of FGFR3 is lost, releasing FGFR3 signaling from miR-99a-de

172 FGFR3 and TP53 mutations is interpretable if FGFR3 is mutated first.

173 The activation of mutant FGFR3 is substantially increased due to a combination of

174 Fibroblast growth factor receptor 3 (FGFR3) is a key regulator of growth and differentiation,

175 Fibroblast growth factor receptor 3 (FGFR3) is a major negative regulator of bone growth that

176 FGF receptor 3 (FGFR3) is activated by mutation or over-expression in ma

177 tion of fibroblast growth factor receptor 3 (FGFR3) is linked to Ras and MAPK activation, therefore c

178 ich any one of three FGFRs (FGFR1, FGFR2, or FGFR3) is sufficient for survival.

179 tion in fibroblast growth factor receptor 3 (FGFR3) is the genetic cause for Crouzon syndrome with Ac

180 cooperation between Fgfr1 and Fgfr2 but not Fgfr3, is required for the initial generation of OLPs in

181 FGF18, a high affinity ligand for FGFR3, is the only FGF-based drug currently in clinical

182 In hepatoma/hepatocarcinoma cell lines, FGFR3 isoforms were overexpressed by lentiviral construc

183 Coexpression of Fgfr3(K650E) and Sox9 in cells resulted in very high lev

184 of thanatophoric dysplasia type II in which FGFR3(K650E) expression was directed to the appendicular

185 Consistent with these in vivo results, FGFR3(K650E) expression was found to increase Sox9 and d

186 Fgfr3(K650E) had opposing effects on Sox9 and beta-caten

187 ch expresses constitutively activated FGFR3 (FGFR3(K650E)) in postmitotic glutamatergic neurons.

188 These results suggest that FGFR3 kinase activity may regulate the PV reproductive p

189 These results imply that the activity of the FGFR3 kinase in the infected epithelial cell restricts t

190 by the fibroblast growth factor receptor 3 (FGFR3) kinase.

191 cell lines expressing constitutively active FGFR3, knockdown of SCD1 by siRNA markedly attenuated ce

192 r (FGFR) KO mice; however, FGFR1, FGFR2, and FGFR3 KO mice did not mimic the phenotype of Fgf2 KO mic

193 In contrast, PLZF loss reduces FGFR3 levels, leading to premature neuronal differentiat

194 ression of FGF10, FGFBP3, FGFR1, FGFR2b, and FGFR3, major local drivers of angiogenesis.

195 l effects and the presence of UTX blocked an FGFR3-mediated increase in the colony formation of bladd

196 Accordingly, blockade of FGFR3-mediated signaling may be a promising therapeutic

197 ion panel including ALK, BRAF, FGFR1, FGFR2, FGFR3, MET, NRG1, NTRK1, NTRK2, NTRK3, RET and ROS1 on e

198 l patterns of COL10A1, SOX9, IHH, PTCH1, and FGFR3 mRNA expression in the growth plate.

199 ections revealed a ~70-fold up-regulation of Fgfr3 mRNA in osteocytes versus osteoblasts of Hyp mice.

200 al" BC cells and it correlated directly with FGFR3 mRNA levels but not with the presence of activatin

201 utant, the C342R FGFR2 mutant, and the C228R FGFR3 mutant.

202 effects of mutant FGFR3, as its knockdown in FGFR3-mutant bladder cancer cell lines is associated wit

203 in patients with FGFR1-amplified sqNSCLC and FGFR3-mutant bladder/urothelial cancer.

204 types, including FGFR1-amplified sqNSCLC and FGFR3-mutant bladder/urothelial cancers.

205 autophagy-independent cell death synergy in FGFR3-mutant cell lines between mTOR (mammalian target o

206 pression of FGFR3b-S249C, the most prevalent FGFR3 mutation in human LGP-UCB, in cultured urothelial

207 nscription and were enriched with activating FGFR3 mutations and potential FGFR inhibitor sensitivity

208 ew experimental evidence indicating that the FGFR3 mutations have very limited urothelial tumorigenic

209 vels but not with the presence of activating FGFR3 mutations.

210 cking FGF2 signaling by central injection of FGFR3-neutralizing antibody was able to reverse the dimi

211 ions of fibroblast growth factor receptor 3 (FGFR3) occur in up to 80% of low-grade papillary urothel

212 By analyzing the effect of the truncated FGFR3 on full-length receptor phosphorylation, we demons

213 r early inner ear development, e.g. Pax8 and Fgfr3 or are expressed in specific hindbrain neurons reg

214 patients with A:T to T:A mutations in TP53, FGFR3, or HRAS.

215 sias similar to those caused by mutations in FGFR3, our results suggest that dysregulation of Sox9 an

216 sing mice carrying a corresponding mutation (FgfR3(P244R) ), we determined whether the mutation affec

217 In FgfR3(P244R) mutants, the condyles displayed reduced lev

218 is of our data indicates that the activating FgfR3(P244R) mutation disturbs TMJ developmental process

219 tion in fibroblast growth factor receptor 3 (FGFR3(P250R) ).

220 , CDK1 and 20-palbociclib, CASP1-imexon, and FGFR3-pazopanib.

221 The current study demonstrates that FGFR3 phosphorylates E2 at tyrosine 138, which inhibits

222 ed that fibroblast growth factor receptor 3 (FGFR3) phosphorylates the viral E2 protein.

223 d that the pan-FGFR TKI, NVP-BGJ398, reduces FGFR3 phosphorylation and corrects the abnormal femoral

224 mutation) and low-risk (presence of ARID1A, FGFR3, PIK3CA, STAG2, and/or TSC1 mutation and absence o

225 Fibroblast growth factor receptor 3 (FGFR3) plays a critical role in the control of endochond

226 0C can influence the alternative splicing of FGFR3 pre-mRNA, supporting a role for some snoRNAs in th

227 tionally opposed FGF10-FGFR2b signaling, and FGFR3 preferentially used downstream phosphoinositide 3-

228 of adipogenesis and involves FGF receptor-3 (FGFR3), prostaglandin-E2 and interaction between estroge

229 roliferation and tumor progression, while WT FGFR3 protein was not tumorigenic, even under forced ove

230 Pharmacological or genetic inhibition of the FGFR3/Ras axis restored the sensitivity of vemurafenib-r

231 Together, we describe a novel FGFR3/Ras mediated mechanism for acquired-resistance to

232 otein (MAP) kinase pathway downstream of the FGFR3 receptor and may also act independently in the gro

233 FGF18, in turn, through binding to its FGFR3 receptor on endothelial cells, can activate the AK

234 Fibroblast growth factor receptor 3 (FGFR3) regulates HPV replication through phosphorylation

235 Chst11, Fgfr3, Runx2 and Runx3 are among many other newly identi

236 Several approaches to reduce FGFR3 signaling by blocking receptor activation or inhib

237 region (3'-UTR) of FGFR3 is lost, releasing FGFR3 signaling from miR-99a-dependent inhibition and gr

238 Furthermore, FGF9-FGFR3 signaling functionally opposed FGF10-FGFR2b signal

239 We found that FGFR3 signaling promotes the cleavage and activation of

240 on, we show that blocking of increased Fgf23-FGFR3 signaling with anti-Fgf23 antibodies or an FGFR3 i

241 GFR3, we identified a gene-signature linking FGFR3 signaling with de novo sterol and lipid biosynthes

242 berrant fibroblast growth factor receptor 3 (FGFR3) signaling disrupts chondrocyte proliferation and

243 ase (Tnap) transcription via FGF receptor-3 (FGFR3) signaling, leading to inhibition of mineralizatio

244 port an inverse correlation between proNodal-FGFR3 signalling and pSmad1/5/8, and show that proNodal-

245 lling and pSmad1/5/8, and show that proNodal-FGFR3 signalling antagonises BMP-mediated pSmad1/5/8 sig

246 Our studies suggest that proNodal/FGFR3 signalling governs Shh duration by repressing cano

247 ETS-family, ETV5, as a putative effector of FGFR3 signalling in bladder cancer.

248 We show that FGFR3 signalling induces a MAPK/ERK-mediated increase in

249 Ps rapidly silence Shh once endogenous Nodal-FGFR3 signalling is downregulated.

250 R1 or FGFR2 amplification (n = 20), FGFR2 or FGFR3 single-nucleotide variants (n = 19), or FGFR1 or F

251 ells in which Fgfr3 expression is reduced by Fgfr3 siRNA fail to bind to proNodal.

252 Finally, targeted electroporation of Fgfr3 siRNA to prechordal mesoderm in vivo results in pr

253 Here, we provide mechanistic insight that FGFR3 splice variants IIIb and IIIc impact considerably

254 FGFR3 strongly associates with these chaperone complexes

255 Additionally, activation of FGFR3 sufficiently reactivated Ras/MAPK signaling and co

256 Subsequently, a survey of FGFR3-TACC3 fusion and other RTK fusions from a large co

257 s, including CRISPR-mediated inactivation of FGFR3-TACC3 fusion genes.

258 rrence and cell line model of the targetable FGFR3-TACC3 fusion in TNBC.

259 issue of the JCI, Parker et al. identify an FGFR3-TACC3 fusion oncogene in glioblastoma and demonstr

260 Validation of FGFR3-TACC3 fusion proteins as endogenous drivers of res

261 Thus, FGFR3-TACC3 fusion proteins may represent a novel mechan

262 ng in resistant cell lines demonstrated that FGFR3-TACC3 fusion proteins promote resistance by prefer

263 Furthermore, although FGFR3-TACC3 fusion proteins promote resistance of additi

264 encing revealed that resistant cells express FGFR3-TACC3 fusion proteins, which were validated as dri

265 entify fusion genes in glioma and discovered FGFR3-TACC3 fusions in 4 of 48 glioblastoma samples from

266 These results demonstrated that the FGFR3-TACC3 gene fusion is expressed in human cancer and

267 ncluding three recurrent fusion transcripts: FGFR3-TACC3, RNF213-SLC26A11, and PTPRZ1-MET (ZM).

268 ongs survival of mice harboring intracranial FGFR3-TACC3-initiated glioma.

269 E2 protein may be regulated through a direct FGFR3 target during the maintenance stage of the PV life

270 ation occurs when the JM domain is linked to FGFR3 TM domain and not simply anchored to the plasma me

271 The pathogenic A391E mutation in FGFR3 TM domain emulates the action of fgf2, trapping th

272 found that FGF9 signaled through epithelial FGFR3 to directly promote distal epithelial fate specifi

273 l transition and a switch from dependency on FGFR3 to ERBB family members.

274 rowth factor receptor (FGFR) genes (FGFR1 or FGFR3) to the transforming acidic coiled-coil (TACC) cod

275 FGFR3-transforming acid coiled coil 3 (TACC3) fusions re

276 al and endometrial cancer (all with FGFR2 or FGFR3 translocations); 16 patients had stable disease.

277 The G380R mutation in FGFR3 transmembrane domain is known as the genetic cause

278 AA-enriched splice variants of PIK3CD, FGFR3, TSC2 and RASGRP2 contribute to greater oncogenic

279 onstrated the expression of FGF21, FGFR1 and FGFR3 (two receptors known to be activated by FGF21) and

280 so known as KDM6A) and activation of the RTK FGFR3, two events that commonly cooccur in muscle invasi

281 co-immunoprecipitate and proNodal increases FGFR3 tyrosine phosphorylation.

282 fibroblast growth factor receptors FGFR2 and FGFR3, tyrosine phosphatase PTPN11, and RAS oncogene hom

283 The data suggest that FGFR3 unliganded dimers are stabilized by receptor-recep

284 GFR3, VEGFR2-FGFR1, VEGFR2-FGFR2, and VEGFR2-FGFR3, using a FRET-based method.

285 mutation at the gatekeeper residue, encoding FGFR3(V555M); consistent with this, KMS-11R cells were c

286 Deregulated FGFR3 variants exhibit specific effects in the malignant

287 The occurrence of FGFR3 variants was analyzed in human HCC samples.

288 actor receptor 1 (FGFR1), EPHA2-FGFR2, EPHA2-FGFR3, VEGFR2-FGFR1, VEGFR2-FGFR2, and VEGFR2-FGFR3, usi

289 Aberrant activation of FGFR3 via overexpression or mutation is a frequent featu

290 In situ hybridization showed that FgfR3 was expressed in condylar chondroprogenitors and m

291 The reduced accumulation of FGFR3 was linked to increased FGFR3 degradation that occ

292 FGFR3 was previously shown to undergo proteolytic cleava

293 Fibroblast growth factor receptor 3 (FGFR3) was also identified as a target of miR-701-3p.

294 subjected to short hairpin RNA knockdown of FGFR3, we identified a gene-signature linking FGFR3 sign

295 ommon bladder cancer mutations like TP53 and FGFR3 were found in organoids in the biobank.

296 imers, with the largest effects observed for FGFR3 wild-type/mutant heterodimers.

297 31 (HPV-31) E2, which also colocalized with FGFR3 within the nucleus.

298 ceptor phosphorylation, we demonstrated that FGFR3 WT/G380R heterodimers form with lower probability

299 Concomitantly, we analyzed the phenotype of Fgfr3(Y367C/+) mice and showed the presence of ACH-relat

300 We found that in Fgfr3(Y367C/+) mice, treatment with this CNP analog led