ライフサイエンスコーパス: growth factor receptor

1 trophic receptor tyrosine kinase 1 and nerve growth factor receptor.

2 RET is a transmembrane growth factor receptor.

3 has been characterized as a mutant epidermal growth factor receptor.

4 e critical for cellular events downstream of growth factor receptors.

5 ignalling) and reduce the desensitization of growth factor receptors.

6 ses as well as of cellular cargos, including growth factor receptors.

7 ck squamous cell cancer, the human epidermal growth factor receptor 1 (EGFR) is the dominant signalin

8 h included enhanced expression of fibroblast growth factor receptor 1 (FGFR1) and axonal guidance mol

9 Hypoxia induced increased fibroblast growth factor receptor 1 (FGFR1) expression in NSCLC cel

10 Mechanistically, fibroblast growth factor receptor 1 (FGFR1) inhibition abolished th

11 r 2 (VEGFR2), EPHA2-VEGFR2, EPHA2-fibroblast growth factor receptor 1 (FGFR1), EPHA2-FGFR2, EPHA2-FGF

12 Insulin-Like Growth Factor Receptor 1 (IGF-1R) and Epidermal Growth F

13 vealing increased expression of insulin-like growth factor receptor 1 (IGF1R).

14 methods predicted that Vascular Endothelial Growth Factor Receptor 1 (VEGFR1) could be one of the po

15 wth factor receptor 2) and FGFR1 (fibroblast growth factor receptor 1) after ischemic stroke.

16 strogen receptors alpha and beta, fibroblast growth factor receptor-1, protein kinase C, and matrix m

17 Cs) express constitutively active fibroblast growth factor receptor 2 (FGFR2) fusion proteins (FFs) g

18 rogen receptor (ER)-positive human epidermal growth factor receptor 2 (HER(2))-negative breast cancer

19 d whether dual versus single human epidermal growth factor receptor 2 (HER2) -targeting drugs added t

20 factor receptor (EGFR), and human epidermal growth factor receptor 2 (HER2) are involved in tumor re

21 ion and/or overexpression of human epidermal growth factor receptor 2 (HER2) are observed in 15-20% o

22 , progesterone receptor, and human epidermal growth factor receptor 2 (HER2) expression, is associate

23 , progesterone receptor, and human epidermal growth factor receptor 2 (HER2) expression, is closely r

24 Overexpression of human epidermal growth factor receptor 2 (HER2) in breast cancer patient

25 ase inhibitor neratinib is a human epidermal growth factor receptor 2 (HER2) inhibitor approved by th

26 sistance of breast cancer to human epidermal growth factor receptor 2 (HER2) inhibitors involves repr

27 Human epidermal growth factor receptor 2 (HER2) is overexpressed in >20%

28 Overexpression of the human epidermal growth factor receptor 2 (HER2) is the cause of HER2-pos

29 Data on human epidermal growth factor receptor 2 (HER2) oncogene overexpression

30 l adenocarcinomas (EACs) are human epidermal growth factor receptor 2 (HER2) positive.

31 ogesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2), are absent is known to

32 Patients are categorized by human epidermal growth factor receptor 2 (HER2), hormone receptor (HR),

33 Human epidermal growth factor receptor 2 (HER2)-amplified breast cancers

34 re, we transiently expressed human epidermal growth factor receptor 2 (HER2)-binding monomeric IgA1,

35 The TEXT/SOFT HR-positive/human epidermal growth factor receptor 2 (HER2)-negative analysis popula

36 CA carriers with stage I-III human epidermal growth factor receptor 2 (HER2)-negative breast cancer.

37 Estrogen receptor-positive/human epidermal growth factor receptor 2 (HER2)-negative cases without c

38 ormone receptor-positive and human epidermal growth factor receptor 2 (HER2)-negative metastatic brea

39 Methods: Patients with ER+/human epidermal growth factor receptor 2 (HER2)-negative metastatic brea

40 pproved for the treatment of human epidermal growth factor receptor 2 (HER2)-negative metastatic brea

41 RCA1/2 mutation (gBRCAm) and human epidermal growth factor receptor 2 (HER2)-negative metastatic brea

42 PET) method in patients with human epidermal growth factor receptor 2 (HER2)-negative, carcinoembryon

43 d treatments for metastatic, human epidermal growth factor receptor 2 (HER2)-positive breast cancer t

44 R2CLIMB study, patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer w

45 patients with stage I to III human epidermal growth factor receptor 2 (HER2)-positive breast cancer w

46 tment of patients with small human epidermal growth factor receptor 2 (HER2)-positive breast cancer.

47 Patients with human epidermal growth factor receptor 2 (HER2)-positive metastatic brea

48 Conclusion Human epidermal growth factor receptor 2 (HER2)-targeted imaging with zi

49 Background Human epidermal growth factor receptor 2 (HER2)-targeted therapies are s

50 cells that are positive for human epidermal growth factor receptor 2 (HER2).

51 wo different epitopes of the human epidermal growth factor receptor 2 (HER2).

52 atures include activation of human epidermal growth factor receptor 2 (HER2, encoded by ERBB2), activ

53 rms of EGFR and its paralog, human epidermal growth factor receptor 2 (HER2/ERBB2) in vesicles derive

54 optosis, and inhibiting vascular endothelial growth factor receptor 2 (VEGFR-2) in endothelial cells.

55 m-SCF/c-Kit and VEGF-A/vascular endothelial growth factor receptor 2 (VEGFR-2), contributing to thei

56 growth factor A (VEGFA)/vascular endothelial growth factor receptor 2 (VEGFR2) signaling is a common

57 sstalk between IL-6 and vascular endothelial growth factor receptor 2 (VEGFR2) signaling pathways in

58 tment after injury; (2) vascular endothelial growth factor receptor 2 (VegfR2) signaling; and (3) Veg

59 y reduced expression of vascular endothelial growth factor receptor 2 (VEGFR2) was established, which

60 l glycoproteins such as vascular endothelial growth factor receptor 2 (VEGFR2) with sialic acid-cappe

61 , which encodes for the Vascular Endothelial Growth Factor Receptor 2 (VEGFR2), as a novel PAH candid

62 ceptor A2 (EPHA2), EGFR-vascular endothelial growth factor receptor 2 (VEGFR2), EPHA2-VEGFR2, EPHA2-f

63 cohort of 156 patients with human epidermal growth factor receptor 2 -negative breast cancer from th

64 lycocalyx regulation of vascular endothelial growth factor receptor 2 activity.

65 n site and the tumor markers human epidermal growth factor receptor 2 and estrogen receptor had an im

66 Ramucirumab-an IgG1 vascular endothelial growth factor receptor 2 antagonist-plus docetaxel was p

67 conditional deletion of vascular endothelial growth factor receptor 2 in vascular endothelial cells a

68 targeted therapies exist for human epidermal growth factor receptor 2 positive (HER2 +) breast cancer

69 umber of biomarkers, such as human epidermal growth factor receptor 2 protein, p53 tumor suppressor g

70 r, progesterone receptor and human epidermal growth factor receptor 2 status and tumor grade.

71 t activation of VEGFR2 (vascular endothelial growth factor receptor 2) and decreases blood levels of

72 their receptors VEGFR2 (vascular endothelial growth factor receptor 2) and FGFR1 (fibroblast growth f

73 europilin-1 and VEGFR2 (vascular endothelial growth factor receptor 2), whereas in the adult LSEC (fe

74 tive for ER and negative for human epidermal growth factor receptor 2, each with characteristic tumou

75 d humanized NSG mice bearing human epidermal growth factor receptor 2-expressing human breast cancer

76 receptor-positive (ER+) and human epidermal growth factor receptor 2-negative (HER2-) breast cancer

77 e receptor greater than 50%; human epidermal growth factor receptor 2-negative breast cancer were ran

78 in the routine treatment of human epidermal growth factor receptor 2-negative early breast cancer (E

79 an effective/safe option in human epidermal growth factor receptor 2-negative EBC with pN0 high geno

80 h hormone receptor-positive, human epidermal growth factor receptor 2-negative, and node-negative bre

81 h hormone-receptor-positive, human epidermal growth factor receptor 2-negative, axillary node-negativ

82 those of triple-negative and human epidermal growth factor receptor 2-positive (HER2+) cancers.

83 ers from triple-negative and human epidermal growth factor receptor 2-positive cancers.

84 T imaging of mouse models of human epidermal growth factor receptor 2-positive or -negative lung canc

85 Human epidermal growth factor receptor 2-positive tumors were excluded.

86 s (VE-cadherin, VEGFR2 [vascular endothelial growth factor receptor 2], or VWF [von Willebrand Factor

87 gesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2) are the three crucial bi

88 gesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2) status.

89 an bind to and activate vascular endothelial growth factor receptor-2 (VEGFR2) in endothelial cells,

90 wth Factor Receptor 1 (IGF-1R) and Epidermal Growth Factor Receptor 3 (ErbB3) have been implicated as

91 we reported that tyrosine kinase fibroblast growth factor receptor 3 (FGFR3) complexes with and phos

92 Other anti-fibroblast growth factor receptor 3 (FGFR3) compounds are showing p

93 PV-31 E2 is phosphorylated by the fibroblast growth factor receptor 3 (FGFR3) kinase.

94 Fibroblast growth factor receptor 3 (FGFR3) regulates HPV replicati

95 Fibroblast growth factor receptor 3 (FGFR3) was also identified as

96 h factor receptor (EGFR) and human epidermal growth factor receptor 3 (HER3) have been investigated a

97 3K interactors, such as the platelet-derived growth factor receptor A (PDGFRA), as well as novel RNA-

98 posure, activated the Dectin-1-SYK-epidermal growth factor receptor-AKT/extracellular signal-regulate

99 enic mutation in the KIT or platelet-derived growth factor receptor alpha (PDGFRA) genes.

100 tyrosine kinase (KIT), and platelet-derived growth factor receptor alpha (PDGFRA) is a clinical chal

101 (ICC), and cells expressing platelet-derived growth factor receptor alpha (PDGFRalpha(+) cells).

102 (ICC), and cells expressing platelet-derived growth factor receptor alpha (PDGFRalpha(+) cells).

103 we investigate the role of platelet-derived growth factor receptor alpha (PDGFRalpha) in the diverge

104 cooperated with activating platelet-derived growth factor receptor alpha (PDGFRalpha) mutant and Trp

105 toresponses, were bred with platelet-derived growth factor receptor alpha (Pdgfralpha)-Cre mice to de

106 IL1B stimulated subsets of platelet-derived growth factor receptor alpha(+) (PDGRFA(+)) fibroblasts

107 ceptors (ARs) expression in platelet-derived growth factor receptor alpha(+) cells (PDGFRalpha(+) cel

108 f enteric neurons, ICC, and platelet-derived growth factor receptor alpha(+) cells were unchanged.

109 ved cells expressing PDGFR (platelet-derived growth factor receptor)-alpha were isolated and differen

110 Platelet-derived growth factor receptor-alpha (PDGFRalpha) is a novel bio

111 ecursor cells by inhibiting platelet-derived growth factor receptor-alpha cell endocytosis.

112 esence and distributions of platelet-derived growth factor receptor-alpha(+) (PDGFRalpha(+) ) ICs in

113 agents that target the vascular endothelial growth factor receptor and a shift in the current standa

114 active, drug-insensitive state by epidermal growth factor receptor and aurora kinase signalling.

115 ted to antibodies that target the epithelial growth factor receptor and excited off-resonance using 7

116 at p-Ezrin (T567) is controlled by epidermal growth factor receptor and MET.

117 nstrated that YAP1 interacted with epidermal growth factor receptor and TGF-beta signaling pathways t

118 cover the oligomeric states of the epidermal growth factor receptor and the secretin receptor in the

119 ing insulin-like growth factor 1, fibroblast growth factor receptor and WNT signalling are similar to

120 mblies are surface-engineered with epidermal growth factor receptors and can be targeted to cancer ce

121 rosine kinase family members EGFR (epidermal growth factor receptor) and Her2 are among the prominent

122 undance of caveolin-1, dystrophin, epidermal growth factor receptor, and insulin receptor-beta; decre

123 The resultant anti-epidermal growth factor receptor (anti-EGFR) AEC worked efficientl

124 al and cancer cells, and MET, the hepatocyte growth factor receptor, are potential targets for therap

125 een Target of Rapamycin (TOR) and Fibroblast growth factor receptor b (Fgfrb) signaling in ring muscl

126 tic loop phosphorylation of platelet-derived growth factor receptor beta (PDGFRbeta), a receptor tyro

127 s (ISMC) with expression of platelet-derived growth factor receptor beta and progressive loss of phen

128 Platelet-derived growth factor receptor-beta (PDGFRbeta) is a receptor ty

129 ed by release of individual platelet-derived growth factor receptor-beta mural pericytes and subseque

130 ural cell pericyte, soluble platelet-derived growth factor receptor-beta(8,18), and regional BBB perm

131 domain-containing adaptor proteins, notably growth factor receptor-bound protein 2 (GRB2) and CRK-li

132 11-kDa is tightly associated with cellular growth factor receptor-bound protein 2 (Grb2) during inf

133 Patients with HER2 3+ overexpression or growth factor receptor-bound protein 7 (Grb7) -positive

134 e the linker for activation of T cells (LAT):growth-factor-receptor-bound protein 2 (Grb2):son of sev

135 Here we focus on the hepatocyte growth factor receptor (c-MET) and the MAP kinase pathwa

136 The human hepatocyte growth factor receptor (c-MET) signaling pathway is dysr

137 rowth factor receptor (EGFR), and hepatocyte growth factor receptor (c-Met), improves the capture of

138 eins, including apolipoprotein E4, epidermal growth factor receptor, CD71 and programmed death-ligand

139 onstrates that Rab7a-mediated trafficking of growth factor receptors controls beta cell survival.

140 However, mutations in the growth factor receptor CSF3R are commonly co-occurrent i

141 corticotroph adenomas include the epidermal growth factor receptor, cyclin-dependent kinases, and he

142 as an essential protein kinase in epidermal growth factor receptor-dependent head and neck squamous

143 The intracellular trafficking of growth factor receptors determines the activity of their

144 ts interaction with CD81 leading endothelial growth factor receptor (EGFR) activation.

145 Here, a six-arginine-tailed anti-epidermal growth factor receptor (EGFR) affibody was employed to e

146 Epidermal growth factor receptor (EGFR) and human epidermal growth

147 irectly bind and activate cellular epidermal growth factor receptor (EGFR) and integrin beta1, respec

148 ts coding for oncoproteins such as epidermal growth factor receptor (EGFR) and MYC can suppress proli

149 ation of the known PTPRJ substrate epidermal growth factor receptor (EGFR) and of other downstream si

150 oss impacts recycling of the RTKs, epidermal growth factor receptor (EGFR) and proto-oncogene c-Met (

151 We apply this model to epidermal growth factor receptor (EGFR) antibodies and find that t

152 The inhibitory epidermal growth factor receptor (EGFR) antibody, cetuximab, is an

153 NSCLC) patient samples, where anti-epidermal growth factor receptor (EGFR) assisted platform were abl

154 Constitutive activation of the epidermal growth factor receptor (EGFR) because of somatic mutatio

155 For example, agents inhibiting the epidermal growth factor receptor (EGFR) benefit many colorectal ca

156 inases, including signaling by the epidermal growth factor receptor (EGFR) family (EGFR1-4 or the hum

157 e and quantitative analyses of the epidermal growth factor receptor (EGFR) in tissues, we generated a

158 that the combination of afatinib (epidermal growth factor receptor (EGFR) inhibitor) and YM155 (inhi

159 Given the pivotal role of epidermal growth factor receptor (EGFR) inhibitors in advanced EGF

160 colorectal cancers unresponsive to epidermal growth factor receptor (EGFR) inhibitors.

161 Mutational activation of the epidermal growth factor receptor (EGFR) is a major player in the p

162 Epidermal growth factor receptor (EGFR) is a prototype receptor ty

163 Epidermal growth factor receptor (EGFR) is commonly over-expressed

164 Asymmetric dimer formation of epidermal growth factor receptor (EGFR) is crucial for EGF-induced

165 We demonstrate that the epidermal growth factor receptor (EGFR) is required as a cofactor

166 c tyrosine residue in STING by the epidermal growth factor receptor (EGFR) is required for directing

167 ch gain-of-function mutants in the epidermal growth factor receptor (EGFR) kinase.

168 genic mice (HBUS) that express the epidermal growth factor receptor (EGFR) ligand HBEGF (heparin-bind

169 Here, we demonstrate that epidermal growth factor receptor (EGFR) ligands can activate the h

170 In epidermal growth factor receptor (EGFR) mutant non-small-cell lung

171 Acquired drug resistance in epidermal growth factor receptor (EGFR) mutant non-small-cell lung

172 The discovery of activating epidermal growth factor receptor (EGFR) mutations spurred the use

173 on of adenocarcinoma histology and epidermal growth factor receptor (EGFR) mutations.

174 PPIN structure and function of the Epidermal Growth Factor Receptor (EGFR) network in colorectal canc

175 ll receptor NKp30 on NK cells with epidermal growth factor receptor (EGFR) on tumor cells in a bispec

176 Overexpression of the epidermal growth factor receptor (EGFR) on various cancers makes i

177 ing mutations in the gene encoding epidermal growth factor receptor (EGFR) or rearrangements in the g

178 utually exclusive mutations in the epidermal growth factor receptor (EGFR) or the guanosine triphosph

179 iated by different factors such as epidermal growth factor receptor (EGFR) overexpression and DNA rep

180 atidylinositol 3-kinase (PI3K) and epidermal growth factor receptor (EGFR) pathway genes are common,

181 posterior, JAK/STAT works with the epidermal growth factor receptor (EGFR) pathway to express the T-b

182 Differential epidermal growth factor receptor (EGFR) phosphorylation is thought

183 We report that epidermal growth factor receptor (EGFR) regulates DNA repair in HS

184 The epidermal growth factor receptor (EGFR) signaling cascade is known

185 For instance, targeting epidermal growth factor receptor (EGFR) signaling is effective in

186 Epidermal growth factor receptor (EGFR) signaling is essential for

187 Epidermal growth factor receptor (EGFR) signaling is initiated by

188 S and discovered that genes of the epidermal growth factor receptor (EGFR) signaling pathway are expr

189 ligomerization domain 2 (NOD2) and epidermal growth factor receptor (EGFR) signaling pathway.

190 liferation in rats is dependent on epidermal growth factor receptor (EGFR) signaling.

191 ncreatitis with hyperactivation of epidermal growth factor receptor (EGFR) signaling.

192 nterleukin 6 receptor (IL-6R), and epidermal growth factor receptor (EGFR) signaling.

193 eaction-diffusion system involving epidermal growth factor receptor (EGFR) signalling interacting wit

194 library of 7,216 randomly mutated epidermal growth factor receptor (EGFR) single-nucleotide variants

195 ion in vitro, and was dependent on epidermal growth factor receptor (EGFR) stimulation.

196 deployment of the first antagonist epidermal growth factor receptor (EGFR) therapeutic antibodies, br

197 d that acquired resistance to anti-epidermal growth factor receptor (EGFR) therapies such as cetuxima

198 Targeting epidermal growth factor receptor (EGFR) through an allosteric mech

199 r dormancy that develops following epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor

200 Several epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors

201 n EMT, we examined the activity of epidermal growth factor receptor (EGFR), a known EMT driver.

202 In comparison to epidermal growth factor receptor (EGFR), a well-established GBM ta

203 RTKs) on host cells, including the epidermal growth factor receptor (EGFR), and activates cellular si

204 CAM), carbonic anhydrase IX (CA9), epidermal growth factor receptor (EGFR), and hepatocyte growth fac

205 cyte growth factor receptor (MET), epidermal growth factor receptor (EGFR), and human epidermal growt

206 grin alpha5beta1, alphavbeta1, and epidermal growth factor receptor (EGFR), and subsequent simultaneo

207 Nuclear RTKs, including the epidermal growth factor receptor (EGFR), are important for process

208 r tyrosine kinases (RTKs), MET and epidermal growth factor receptor (EGFR), are known to play a criti

209 Inhibition of epidermal growth factor receptor (EGFR), extracellular signal-regu

210 position and tissue expression of epithelial growth factor receptor (EGFR), IL-33 and receptor ST2 we

211 rosine kinases (RTKs), such as the epidermal growth factor receptor (EGFR), locally increases the abu

212 a signaling cascade that includes epidermal growth factor receptor (EGFR), signal transducer and act

213 ly (ADP-ribose) polymerase (PARP), epidermal growth factor receptor (EGFR), Vascular endothelial grow

214 The epidermal growth factor receptor (EGFR), when carrying an activati

215 cally in cells over-expressing the epidermal growth factor receptor (EGFR), with over 99% reduction i

216 attenuation of the pro-tumorigenic Epidermal Growth Factor Receptor (EGFR)-Akt axis, and finally cell

217 all-cell lung cancer (NSCLC) is an epidermal growth factor receptor (EGFR)-directed oral tyrosine kin

218 n in a Drosophila genetic model of epidermal growth factor receptor (EGFR)-driven tumorigenesis simil

219 erointeractions of nine RTK pairs, epidermal growth factor receptor (EGFR)-EPH receptor A2 (EPHA2), E

220 a connection that upregulation of epidermal growth factor receptor (EGFR)-leukemia inhibitory factor

221 ion-mediated apoptosis by p53- and epidermal growth factor receptor (EGFR)-mediated DNA repair.

222 Epidermal growth factor receptor (EGFR)-targeted therapy in non-sm

223 lude the tetraspanin CD151 and the epidermal growth factor receptor (EGFR).

224 hich, in turn, is regulated by the epidermal growth factor receptor (EGFR).

225 ncing KSHV infectivity through the epidermal growth factor receptor (EGFR).

226 nded on the transactivation of the epidermal growth factor receptor (EGFR).

227 body cetuximab and its target, the epidermal growth factor receptor (EGFR).

228 egy for tumours overexpressing the epidermal growth factor receptor (EGFR).

229 We found that epidermal growth factor receptor (EGFR)/BRAF inhibition down-regul

230 ERBB4 is a member of the epidermal growth factor receptor (EGFR)/ERBB subfamily of receptor

231 mation, we identify a role for the epidermal growth factor receptor (EGFR/ERBB1) as a mediator of cor

232 The human epidermal growth factor receptor (EGFR/ERBB1) is a receptor tyrosi

233 wild-type patients (patients with epidermal growth factor receptor [EGFR] or anaplastic lymphoma kin

234 significantly expressed fewer transcripts of growth factor receptors, EGFR, FGFR1, and FGRF2 than U c

235 oring actionable aberration(s) in fibroblast growth factor receptor (FGFR) 1-3 were treated with AZD4

236 Fibroblast growth factor receptor (FGFR) 2 gene alterations are inv

237 We assessed actions of fibroblast growth factor receptor (FGFR) 2 in urothelium after cycl

238 ucture of sKlotho in complex with fibroblast growth factor receptor (FGFR) and fibroblast growth fact

239 e is defined by activation of the fibroblast growth factor receptor (FGFR) pathway and this subtype i

240 Aberrant activation of fibroblast growth factor receptor (FGFR) signalling contributes to

241 force transduction or initiating fibroblast growth factor receptor (FGFR)-dependent biochemical sign

242 tional optogenetic design for the fibroblast growth factor receptor (FGFR).

243 In contrast, fibroblast growth factor receptors (FGFRs) recruit Fibroblast Growt

244 in]; and 3 with lower risk: ErbB1 [epidermal growth factor receptor], GDF-11/8 [growth differentiatio

245 raditional chemical and anti-human epidermal growth factor receptor (HER) treatments.

246 minal A-like, luminal B-like human epidermal growth factor receptor (HER)2-negative/HER2-positive, HE

247 ormed the human insulin (hIR) and hepatocyte growth factor receptor (hMET) into glutamate receptors b

248 Epidermal growth factor receptor I (EGFR) is overexpressed in most

249 n beta cells and increases expression of the growth factor receptors IGF-1R and c-Met.

250 hioredoxin and peroxiredoxin, as well as the growth factor receptors IGF1R and ERBB3.

251 x formation and the degradation of epidermal growth factor receptor in the multivesicular body pathwa

252 Cetuximab, an epidermal growth factor receptor inhibitor, has been proposed for

253 Lapatinib, an approved epidermal growth factor receptor inhibitor, was explored as a star

254 p elicit optimal receptor-ligand activity of growth factor receptors, integrins, integrin ligands, le

255 n particular, the compensatory activation of growth factor receptors leads to chemoresistance and lim

256 ation by an indirect activation of epidermal growth factor receptor mediated by metalloproteinases.

257 dothelial growth factor-vascular endothelial growth factor receptor-mediated angiogenic signaling, li

258 osstalk between the oncogenic RTK hepatocyte growth factor receptor (MET), epidermal growth factor re

259 n by downregulating the E-cadherin/epidermal growth factor receptor/mitogen-activated protein kinase

260 expression of numerous genes including nerve growth factor receptor (NGFR), which becomes transcripti

261 ents without driver alterations in epidermal growth factor receptor or ALK.

262 other receptors, such as CXCR4, endothelial growth factor receptor, or the alpha (1)-adrenergic rece

263 Platelet Derived Growth Factor Receptor (PDGFR) signaling is a central mi

264 Platelet-derived growth factor receptor (PDGFR)-alpha plays roles in cell

265 ecently discovered that the platelet-derived growth factor receptor(PDGFR)-beta signaling system is b

266 tor neuropilin1 (NRP1), and platelet-derived growth factor receptor (PDGFRalpha and PDGFRbeta).

267 e progenitors (APs) express platelet-derived growth factor receptors (PDGFRs), PDGFRalpha and PDGFRbe

268 e injured kidney, including Smad3, epidermal growth factor receptor, platelet-derived growth factor r

269 cording to cytokeratins 5/6 and/or epidermal growth factor receptor positivity by immunohistochemistr

270 MM function or expression promoted epidermal growth factor receptor-regulated MMP-9 expression via ER

271 mal growth factor receptor, platelet-derived growth factor receptor, signal transducer and activator

272 ll-extracellular matrix signaling, epidermal growth factor receptor signaling, and Rho-GTPase signali

273 ion of effector pathways including epidermal growth factor receptor signaling, extracellular matrix p

274 iderably impairing the extent and quality of growth factor receptor signaling.

275 igen and a concomitant increase in epidermal growth factor receptor signaling.

276 is selectively mediated by platelet-derived growth factor receptor signaling.

277 gnaling by inhibitors of the EGFR (epidermal growth factor receptor) signaling pathway-identified by

278 hed ctDNA-positive CSF-tumour pairs, whereas growth factor receptor signalling pathways showed consid

279 via chemokine C-X-C receptor 4 and epidermal growth factor receptor signalling, including extracellul

280 ied EHD1 (Eps15 [endocytic adaptor epidermal growth factor receptor substrate 15] homology domain-con

281 factor receptors (FGFRs) recruit Fibroblast Growth Factor Receptor Substrate 2 (Frs2) and Rous sarco

282 everely disrupt PM association of fibroblast growth factor receptor substrate 2alpha but do not elimi

283 pidation-deficient mutants of the fibroblast growth factor receptor substrate 2alpha.

284 on of therapeutically important cytokine and growth factor receptor systems.

285 omplementary to VEGF-R (vascular endothelial growth factor receptor)-targeted therapies.

286 Targeting USP8 can reduce the expression of growth factor receptors that participate in cSCC develop

287 omarkers of acquired resistance to Epidermal Growth Factor Receptor therapy.

288 lore the novel hypothesis that regulation of growth factor receptor trafficking can be used to promot

289 nuclide molecular imaging of human epidermal growth factor receptor type 2 (HER2) expression may help

290 (131)I-GMIB-anti-human epidermal growth factor receptor type 2 (HER2)-VHH1 is a targeted

291 pe, grade, hormone receptor, human epidermal growth factor receptor type 2/neu, Ki-67) were extracted

292 on, CNS-active, irreversible, oral epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-T

293 e treatment of advanced progressed epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-

294 entifying responders to vascular endothelial growth factor receptor tyrosine kinase inhibitors and ma

295 lyzed to map the safety profile of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-

296 The oncogene epidermal growth factor receptor variant III (EGFRvIII) is frequen

297 static RCC treated with vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor

298 y process controlled by vascular endothelial growth factor receptor (VEGFR)-Notch signaling.

299 Expression of insulin receptor and epidermal growth factor receptor was reduced in hippocampal neuros

300 he inhibition of its family member epidermal growth factor receptor with small-molecule inhibitors.