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 ondroplasia disorders caused by mutations in FGFR3.

7 3, TRAF3, FAM46C, DIS3, BRAF, LTB, CYLD, and FGFR3.

8 R mutant resistant cancer with a mutation in FGFR3.

9 y enhancing tumor progression relative to WT FGFR3.

10 critical tyrosines in the activation loop of FGFR3.

11 in skeletal diseases caused by mutations in FGFR3.

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

13 ase CHIP is able to interact and destabilize FGFR3.

14 FGFR3 and reduces the signaling capacity of FGFR3.

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

16 regulated intramembrane proteolysis (RIP) of FGFR3.

17 ndividuals express both wild-type and mutant FGFR3.

18 e focused on reducing signals emanating from FGFR3.

19 g point mutations or increased expression of FGFR3.

20 tively activated fusion tyrosine kinase, TEL-FGFR3.

21 or models bearing either wild-type or mutant FGFR3.

22 nd epithelial cancers driven by WT or mutant FGFR3.

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

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

25 therapies target the extracellular domain of FGFR3.

26 prevents ligands from binding and activating FGFR3.

27 to skeletal pathology caused by mutations in FGFR3.

28 s of evidence suggest that proNodal acts via FGFR3.

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

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

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

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

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

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

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

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

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

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

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

40 3 gene was replaced with human FGFR3(G380R) (FGFR3(ACH)) cDNA, the most common mutation in human ACH.

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

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

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

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

45 e investigate the effect of this mutation on FGFR3 activation in HEK 293 T cells over a wide range 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 as/ERK/MAPK pathway may exist in response to FGFR3 activity and identifies a novel therapeutic target

49 Instead, FGFR3 activity in achondroplasia is increased due to inc

50 We also showed that increased FGFR3 activity was sufficient to induce FOXN1 expression

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

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

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

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

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

56 uncovered a positive regulatory loop between FGFR3 and FOXN1 that underlies a benign versus malignant

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

58 bladder cancer, the functional importance of FGFR3 and its potential as a specific therapeutic target

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

60 FGFR3 and p85 proteins also interact in MM cell lines wh

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

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

63 yeloma associated with ectopic expression of FGFR3 and t(4;12)(p16;p13) acute myeloid leukemia associ

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

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

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

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

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

69 the tyrosine kinase receptor FGF receptor-3 (FGFR3) and the transcription factor forkhead box N1 (FOX

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

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

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

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

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

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

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

77 results indicate that the effects of mutant FGFR3 are both cell type specific and mutation specific.

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

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

80 ions of fibroblast growth factor receptor 3 (FGFR3) are frequent in bladder tumors, little informatio

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

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

83 d myeloproliferative syndrome induced by TEL-FGFR3 as compared with wild-type cells, suggesting a cri

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

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

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

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

88 antibody (R3Mab) that inhibited not only WT FGFR3, but also various mutants of the receptor, includi

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

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

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

92 ProNodal and FGFR3 co-immunoprecipitate and proNodal increases FGFR3

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

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

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

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

100 K2 and that this association is required for FGFR3-dependent phosphorylation of RSK2 at Y529 and Y707

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

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

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

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

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

106 suggests that the mutation does not increase FGFR3 dimerization, as proposed previously.

107 We recently reported that FGFR3 directly tyrosine phosphorylates RSK2 at Y529, whi

108 The interaction of p85 with FGFR3 does not require PLCgamma, suggesting the p85 inte

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

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

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

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

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

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

115 aphy revealed that R3Mab bound to a specific FGFR3 epitope that simultaneously blocked ligand binding

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

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 g, as well as accelerated down-regulation of FGFR3 expression, decreased BrdU incorporation and highe

120 ke tumor phenotype, which included increased FGFR3 expression.

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 ed specific shRNA probes to demonstrate that FGFR3 functions as an important driver of bladder carcin

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

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

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

137 ain-of-function mutations in FGF receptor 3 (FGFR3) have been implicated in severe skeletal dysplasia

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

139 g signal transduction pathways downstream of FGFR3 holds promise with the discovery that administrati

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

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

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

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

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

147 FGFR3-IIIb overexpression occurred significantly more of

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

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

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

151 evidence demonstrating an oncogenic role of FGFR3 in bladder cancer and support antibody-based targe

152 tralizing antibodies, designed for targeting FGFR3 in cancer, are still in the preclinical phase and

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 ncer and support antibody-based targeting of FGFR3 in hematologic and epithelial cancers driven by WT

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

157 asure the activation of wild-type and mutant FGFR3 in mammalian cells using Western blots, and we ana

158 contrast to TERT-NHUC, expression of mutant FGFR3 in NIH-3T3 resulted in phosphorylation of Src and

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

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

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

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

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

164 Inhibition of FGFR3 increased target cell apoptosis through the suppre

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

166 cells, suggesting a critical role of RSK2 in FGFR3-induced hematopoietic transformation.

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

168 el antagonist of FGFR3 signaling, useful for FGFR3 inhibition alone or in combination with inhibitors

169 FGFR3 inhibition in these cells inhibits proliferation a

170 3 signaling with anti-Fgf23 antibodies or an FGFR3 inhibitor partially restored the suppression of Tn

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

172 ogenous negative regulatory role for the p85-FGFR3 interaction on the Ras/ERK/MAPK pathway may exist

173 Moreover, we found that FGFR3 interacts with RSK2 through residue W332 in the li

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

175 FGFR3 is expressed in proliferating chondrocytes of the

176 While FGFR3 is frequently overexpressed and/or activated throu

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

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

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

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

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

182 Fibroblast growth factor receptor 3 (FGFR3) is a receptor tyrosine kinase that plays an impor

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

184 Overexpression of FGF receptor 3 (FGFR3) is implicated in the development of t(4;14)-posit

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

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

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

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

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

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

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

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

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

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

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

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

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

198 A unique anti-FGFR3 mAb was shown to exhibit antitumor activity in hum

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

200 and murine limb organ culture, NF449 rescued FGFR3-mediated extracellular matrix loss and growth inhi

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

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

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

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

205 y of both wild type and a disease-associated FGFR3 mutant (K650E) in a fashion that appeared non-comp

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

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

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

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

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

211 enotypic and signaling consequences of three FGFR3 mutations (S249C, Y375C, and K652E) in immortalize

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

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

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

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

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

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

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

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

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

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

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

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

224 -mediated association of FGFRs with p85, the FGFR3-p85 interaction we observed requires FGFR3 Y760, p

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

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

227 kinase fibroblast growth factor receptor 3 (FGFR3) plays a pathogenic role in a number of human hema

228 0C can influence the alternative splicing of FGFR3 pre-mRNA, supporting a role for some snoRNAs in th

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 The FGFR3 receptor tyrosine kinase represents an attractive

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

236 e myeloma xenografts in mice by antagonizing FGFR3 signaling and eliciting antibody-dependent cell-me

237 liferation and induces apoptosis, validating FGFR3 signaling as a therapeutic target in t(4;14) MM ca

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

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

240 nt two major cellular phenotypes of aberrant FGFR3 signaling in cartilage.

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

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

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

244 data identify NF449 as a novel antagonist of FGFR3 signaling, useful for FGFR3 inhibition alone or in

245 named NF449 with inhibitory activity toward FGFR3 signaling.

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

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

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

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

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

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

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

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

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

255 FGFR3 strongly associates with these chaperone complexes

256 irst-generation therapies directly targeting FGFR3, such as kinase inhibitors and neutralizing antibo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 tion in Fibroblast Growth Factor Receptor 3 (FGFR3) that causes achondroplasia suggests that disease

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

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

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

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

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

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

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

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

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

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

285 Deregulated FGFR3 variants exhibit specific effects in the malignant

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

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

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

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

290 FGFR3 was previously shown to undergo proteolytic cleava

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

292 In addition, all forms of mutant FGFR3 were able to phosphorylate Plcgamma1 and induce mo

293 g and undetectable in cells expressing K652E FGFR3, which failed to phosphorylate PLCgamma1.

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

295 The interaction of FGFR3 with p85 is dependent upon receptor activation.

296 31 (HPV-31) E2, which also colocalized with FGFR3 within the nucleus.

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

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

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

300 e FGFR3-p85 interaction we observed requires FGFR3 Y760, previously identified as a PLCgamma binding