ライフサイエンスコーパス: epidermal growth factor

1 diac myofibroblasts secrete milk fat globule-epidermal growth factor 8 (MFG-E8), which promotes apopt

2 tegrin-beta3 and its ligand milk fat globule-epidermal growth factor 8 protein and enhanced efferocyt

3 bined with transforming growth factor-beta1, epidermal growth factor, and IFN-gamma administration, w

4 nation of IRDye 800-labeled therapeutic anti-epidermal growth factor antibody (cetuximab) showed sign

5 nted with a p38 MAPK signaling inhibitor and epidermal growth factor co-treatment.

6 erozygosity for collagen and calcium-binding epidermal growth factor domain-containing protein 1 (CCB

7 We show that ErbB2, which can mediate epidermal growth factor (EGF) and neuregulin signalling

8 yanide or hydrogen peroxide as controls, and epidermal growth factor (EGF) as a physiologically-relev

9 somes and show preferential association with epidermal growth factor (EGF) but not transferrin (Tf) t

10 Lamellipodin mediates directional sensing of epidermal growth factor (EGF) gradients and invasive 3D

11 Stimulation of cells with epidermal growth factor (EGF) induces internalization an

12 Two-color imaging of epidermal growth factor (EGF) ligand and clathrin reveal

13 n of EGFR, HER2, and HER3 in response to the epidermal growth factor (EGF) ligand, while also inhibit

14 variety of molecular pathways, including the epidermal growth factor (EGF) pathway.

15 colorectal cancer cells to drugs that block epidermal growth factor (EGF) receptor signaling could b

16 cells, in which treatment with Dkk1 induced epidermal growth factor (EGF) secretion.

17 sforming growth factor alpha (TGF-alpha) and epidermal growth factor (EGF) share the same EGF recepto

18 Here, we uncovered a central role for epidermal growth factor (EGF) signaling during in vivo n

19 We also demonstrate that epidermal growth factor (EGF) stabilizes PD-L1 via GSK3b

20 Following epidermal growth factor (EGF) stimulation, activated ERK

21 Epidermal growth factor (EGF) was found to stimulate CAR

22 a positive feedback loop involving enhanced epidermal growth factor (EGF)-dependent Akt/GSK3beta pho

23 s that promotes substrates binding to F-box, epidermal growth factor (EGF)-induced c-Fos S374 phospho

24 directed against the four highly constrained epidermal growth factor (EGF)-like domains of Pfs25 bloc

25 Heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF)

26 osphorylation site of NFAT3 was critical for epidermal growth factor (EGF)-stimulated cell transforma

27 ich correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated cells.

28 reduces Ras membrane localization, inhibits epidermal growth factor (EGF)-stimulated Ras signaling a

29 eurons, with a secreted differentiation cue, epidermal growth factor (EGF).

30 Growth factors of the epidermal growth factor (EGF)/neuregulin family are invo

31 herin, which prevents secretion of mitogenic epidermal growth factors (EGFs) by repressing transcript

32 Milk fat globule epidermal growth factor-factor 8 (MFG-E8) is a periphera

33 we found that amphiregulin, a member of the epidermal growth factor family, was prominently up-regul

34 tically engineered BLNs, which display human epidermal growth factor (hEGF) or anti-HER2 Affibody as

35 nfirmed, hormone receptor-positive and human epidermal growth factor (HER2)-negative inoperable local

36 -4, IL-6, IL-8, tumor necrosis factor-alpha, epidermal growth factor, IL-13, IL-17, IL-1alpha, and in

37 asive breast cancer cells, where it mediates epidermal growth factor-induced cortactin tyrosine phosp

38 2-O-Bn-InsP5 is able to inhibit the epidermal growth factor-induced PLCgamma1 phosphorylatio

39 d a role for MIG6 as a negative regulator of epidermal growth factor-induced signaling and cell migra

40 activation of these protein kinases by human epidermal growth factor, insulin, and insulin-like growt

41 Epidermal growth factor is released from stressed cells

42 O-Linked fucose modifications on Notch1 epidermal growth factor-like (EGF) domains 8 and 12 enga

43 Epidermal growth factor-like (EGF) repeats are also smal

44 h activity by modifying O-fucose residues on epidermal growth factor-like (EGF) repeats of Notch.

45 Heparin binding epidermal growth factor-like growth factor (HB-EGF) is a

46 Here we identify heparin-binding epidermal growth factor-like growth factor (HBEGF) as a

47 Heparin-binding epidermal growth factor-like growth factor promotes neur

48 Neuregulin 4 (NRG4), an epidermal growth factor-like signaling molecule, plays a

49 We further show that epidermal growth factor or FBS stimulation induces assoc

50 to receptor tyrosine kinase agonists such as epidermal growth factor or insulin.

51 ctodomain sensitivity of neuregulin-1 (NRG1; epidermal-growth-factor) or CD44 (receptor-tyrosine-kina

52 wth factor, several tyrosine kinase ligands (epidermal growth factor, platelet-derived growth factor,

53 he molecular testing of CRC tissues to guide epidermal growth factor receptor (EGFR) -targeted therap

54 d to evaluate Schwann cell proliferation and epidermal growth factor receptor (EGFR) activation in th

55 Inhibition of inflammation or epidermal growth factor receptor (EGFR) activity decreas

56 an adhesion-independent manner by dampening Epidermal Growth Factor Receptor (EGFR) activity.

57 sary but not sufficient for response to anti-epidermal growth factor receptor (EGFR) agents in advanc

58 oteins gB and gH signal through the cellular epidermal growth factor receptor (EGFR) and alphavbeta3

59 ors, we document that HCMV activation of the epidermal growth factor receptor (EGFR) and downstream p

60 cation, through engagement and activation of epidermal growth factor receptor (EGFR) and integrins on

61 on, Th2 cells required the expression of the epidermal growth factor receptor (EGFR) and of its ligan

62 upstream effector, the role of NDRG1 on the epidermal growth factor receptor (EGFR) and other member

63 seek to characterize the interaction between epidermal growth factor receptor (EGFR) and the cytoplas

64 motes translation of certain mRNAs including epidermal growth factor receptor (EGFR) and the Hippo pa

65 In the model, epidermal growth factor receptor (EGFR) and vascular end

66 has also been proven to positively regulate epidermal growth factor receptor (EGFR) and WNT signalin

67 Mutations in K-Ras and epidermal growth factor receptor (EGFR) are mutually exc

68 BACKGROUND & AIMS: Inhibitors of the epidermal growth factor receptor (EGFR) are the first-li

69 Aberrant amplification and mutations of epidermal growth factor receptor (EGFR) are the most com

70 or receptor bound 2 (GRB2) to phosphorylated epidermal growth factor receptor (EGFR) as a model syste

71 cally interact, we searched for modifiers of epidermal growth factor receptor (EGFR) dependency by pe

72 Epidermal growth factor receptor (EGFR) family members p

73 ressed in keratinocytes, where together with epidermal growth factor receptor (EGFR) forms a signalin

74 ce of this interaction is the removal of the epidermal growth factor receptor (EGFR) from the surface

75 0 and CIN85, which results in the removal of epidermal growth factor receptor (EGFR) from the surface

76 o detect mutations of exons 19 and 21 of the epidermal growth factor receptor (EGFR) gene.

77 Epidermal growth factor receptor (EGFR) has been implica

78 Current knowledge suggests a role for epidermal growth factor receptor (EGFR) in cholangiocyte

79 Despite a well-established role for the epidermal growth factor receptor (EGFR) in tumorigenesis

80 The role of epidermal growth factor receptor (EGFR) inhibition in ch

81 ) patients treated with the third-generation epidermal growth factor receptor (EGFR) inhibitor rocile

82 iRNA signature predictive of response to the epidermal growth factor receptor (EGFR) inhibitor, erlot

83 Reversible epidermal growth factor receptor (EGFR) inhibitors promp

84 neration therapies, overcoming resistance to epidermal growth factor receptor (EGFR) inhibitors remai

85 Epidermal growth factor receptor (EGFR) interacts with i

86 of ubiquitin interaction for the sorting of epidermal growth factor receptor (EGFR) into ILVs for ly

87 The specific targeting of oncogenic mutant epidermal growth factor receptor (EGFR) is a breakthroug

88 The epidermal growth factor receptor (EGFR) is a clinically

89 The epidermal growth factor receptor (EGFR) is a prototypica

90 The epidermal growth factor receptor (EGFR) is a receptor ty

91 Epidermal growth factor receptor (EGFR) is central to ep

92 ecific DNA demethylation and upregulation of epidermal growth factor receptor (EGFR) ligands amphireg

93 roteases are the enzymes that release active epidermal growth factor receptor (EGFR) ligands in Droso

94 paring the concurrent administration of anti-epidermal growth factor receptor (EGFR) monoclonal antib

95 paring the concurrent administration of anti-epidermal growth factor receptor (EGFR) monoclonal antib

96 ll-cell lung cancer patients with activating epidermal growth factor receptor (EGFR) mutations typica

97 small-cell lung carcinoma (NSCLC) harbouring epidermal growth factor receptor (EGFR) mutations.

98 Here, using a beta-cell specific epidermal growth factor receptor (EGFR) null mouse, we s

99 8% (96/348) of patients were found to harbor epidermal growth factor receptor (EGFR) or Kristen rat s

100 Different data support a role for the epidermal growth factor receptor (EGFR) pathway during l

101 accompanied by an increase in the levels of epidermal growth factor receptor (EGFR) phosphorylation,

102 epithelial cells had elevated ligand-induced epidermal growth factor receptor (EGFR) phosphorylation.

103 The epidermal growth factor receptor (EGFR) plays a critical

104 ogeneous expression of amplified and mutated epidermal growth factor receptor (EGFR) presents a subst

105 Epidermal growth factor receptor (EGFR) regulates many c

106 ular endothelial growth factor (VEGFR)-2 and epidermal growth factor receptor (EGFR) signaling by enh

107 Epidermal growth factor receptor (EGFR) signaling has a

108 Epidermal growth factor receptor (EGFR) signaling is a k

109 Epidermal Growth Factor Receptor (EGFR) signaling is ess

110 In addition, epidermal growth factor receptor (EGFR) signaling is reg

111 Aberrant epidermal growth factor receptor (EGFR) signaling is wid

112 Focusing on the epidermal growth factor receptor (EGFR) signaling networ

113 e stem cells (FSCs) of the Drosophila ovary, Epidermal Growth Factor Receptor (EGFR) signaling promot

114 Despite decades of research in the epidermal growth factor receptor (EGFR) signalling field

115 signalosome to prevent ectopic expression of Epidermal growth factor receptor (EGFR) target genes.

116 rized a bi-functional molecule comprising of epidermal growth factor receptor (EGFR) targeted nanobod

117 l-validated solid tumor targets, such as the epidermal growth factor receptor (EGFR) that effectively

118 Current anti-epidermal growth factor receptor (EGFR) therapy for oral

119 tamer previously selected for binding to the epidermal growth factor receptor (EGFR) to create a bifu

120 Here, we find that LOX regulates the epidermal growth factor receptor (EGFR) to drive tumour

121 Signaling from epidermal growth factor receptor (EGFR) to extracellular

122 Epidermal growth factor receptor (EGFR) tyrosine kinase

123 Third-generation epidermal growth factor receptor (EGFR) tyrosine kinase

124 ER-MVB contacts additionally function in epidermal growth factor receptor (EGFR) tyrosine kinase

125 improved progression-free survival with the epidermal growth factor receptor (EGFR) tyrosine kinase

126 EGFR Thr790Met mutation after treatment with epidermal growth factor receptor (EGFR) tyrosine-kinase

127 Here, we show that lnc-epidermal growth factor receptor (EGFR) upregulation in

128 Interferon gamma (IFNgamma) and the epidermal growth factor receptor (EGFR) utilize Janus ki

129 Stimulation of the epidermal growth factor receptor (EGFR) with EGF, the be

130 of CETN3 and SKP1 to elevated expression of epidermal growth factor receptor (EGFR), and SKP1 loss a

131 regulate chloride secretion, centred on the epidermal growth factor receptor (EGFr), are discussed.

132 the wound repair pathway, controlled by the epidermal growth factor receptor (EGFR), is critical to

133 EMMs of lung adenocarcinoma driven by mutant epidermal growth factor receptor (EGFR), mutant Kirsten

134 o may benefit from therapies that target the epidermal growth factor receptor (EGFR), such as cetuxim

135 ve been reported to regulate the function of epidermal growth factor receptor (EGFR), the effect of p

136 verexpression lead to aberrant activation of epidermal growth factor receptor (EGFR), which subsequen

137 ell lines, which was accompanied by enhanced epidermal growth factor receptor (EGFR)-mediated mitogen

138 lthough mechanisms of acquired resistance of epidermal growth factor receptor (EGFR)-mutant non-small

139 ing brain and leptomeningeal metastases-from epidermal growth factor receptor (EGFR)-mutant non-small

140 rsor cells, a well-characterized paradigm of epidermal growth factor receptor (EGFR)-Ras-ERK signalin

141 (SRS), whole-brain radiotherapy (WBRT), and epidermal growth factor receptor (EGFR)-tyrosine kinase

142 f the gene encoding receptor tyrosine kinase epidermal growth factor receptor (EGFR).

143 onformation of the external (ecto) domain of Epidermal Growth Factor Receptor (EGFR).

144 e demonstrated that RCN2 interacted with the epidermal growth factor receptor (EGFR).

145 pecific interaction of an engineered gD with epidermal growth factor receptor (EGFR).

146 eceptor-alpha and reciprocal upregulation of epidermal growth factor receptor (EGFR).

147 ment is driven by detachment-induced loss of epidermal growth factor receptor (EGFR).

148 ped them into siRNA carriers targeted to the epidermal growth factor receptor (EGFR).

149 g by ADAMs [e.g., ligands and receptors from epidermal growth factor receptor (EGFR)/ErbB and tumor n

150 The epidermal growth factor receptor (EGFR)/ErbB family of r

151 ntibodies that intercept a cognate receptor, epidermal growth factor receptor (EGFR)/ERBB1, or a co-r

152 d to letrozole with or without lapatinib, an epidermal growth factor receptor (EGFR)/HER2 tyrosine ki

153 es ErbB signaling by inhibiting formation of epidermal growth factor receptor (EGFR)/human epidermal

154 protein kinase CK2 and the wild-type/mutated epidermal growth factor receptor (EGFR/EGFRvIII), which

155 on of glioblastoma cells expressing a mutant epidermal growth factor receptor (EGFRvIII) is responsib

156 nests that can mediate signals via the human epidermal growth factor receptor (ErbB) tyrosine kinase

157 rst-line chemotherapy is beneficial in human epidermal growth factor receptor (HER) 1/HER2-positive m

158 n G2 monoclonal antibody that binds to human epidermal growth factor receptor (HER) 3 (ErbB3), blocki

159 ons between the catalytically impaired human epidermal growth factor receptor (HER3/ERBB3) and its ca

160 ssion of the receptor tyrosine kinases (RTK) epidermal growth factor receptor 1 (EGFR) and human epid

161 3.80; 95% CI, 2.46-5.87; P < .001) and human epidermal growth factor receptor 2 (ERBB2 [formerly HER2

162 first-line treatment for patients with human epidermal growth factor receptor 2 (HER2) -overexpressin

163 astuzumab to adjuvant chemotherapy for human epidermal growth factor receptor 2 (HER2) -positive earl

164 TCO was conjugated to the anti-human epidermal growth factor receptor 2 (HER2) Affibody molec

165 pidermal growth factor receptor (EGFR)/human epidermal growth factor receptor 2 (HER2) and HER2/HER3

166 her members of the ErbB family, namely human epidermal growth factor receptor 2 (HER2) and human epid

167 By simultaneously targeting the human epidermal growth factor receptor 2 (HER2) expressed by c

168 An example is human epidermal growth factor receptor 2 (HER2) overexpressing

169 e receptor expression and negative for human epidermal growth factor receptor 2 (HER2) overexpression

170 HC) profile, tumors were classified as human epidermal growth factor receptor 2 (HER2) positive (n =

171 sed, histopathologic classification of human epidermal growth factor receptor 2 (HER2) status in wome

172 Human epidermal growth factor receptor 2 (HER2) status is one

173 ght biomarker subtypes on the basis of human epidermal growth factor receptor 2 (HER2) status, hormon

174 the basis of hormone receptor (HR) and human epidermal growth factor receptor 2 (HER2) status.

175 Dual human epidermal growth factor receptor 2 (HER2) targeting can

176 rican Pathologists recommendations for human epidermal growth factor receptor 2 (HER2) testing in bre

177 dy against the extracellular domain of human epidermal growth factor receptor 2 (HER2), 3 other HER2-

178 or for the detection and estimation of human epidermal growth factor receptor 2 (HER2), a biomarker f

179 The sensitive quantification of Human Epidermal growth factor Receptor 2 (HER2), as a key prog

180 on the basis of status with regard to human epidermal growth factor receptor 2 (HER2), hormone recep

181 vely decreased its activity toward the human epidermal growth factor receptor 2 (HER2)- pY(1196) site

182 A-like tumors, 70.5% of luminal B-like human epidermal growth factor receptor 2 (HER2)-negative tumor

183 patient has hormone receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative, node

184 ts with hormone receptor (HR)-negative human epidermal growth factor receptor 2 (HER2)-positive (1.1%

185 r- and progesterone receptor-negative, human epidermal growth factor receptor 2 (HER2)-positive breas

186 and chemotherapy for the treatment of human epidermal growth factor receptor 2 (HER2)-positive breas

187 ncluding adjuvant targeted therapy for human epidermal growth factor receptor 2 (HER2)-positive breas

188 In human epidermal growth factor receptor 2 (HER2)-positive breas

189 In neoadjuvant trials, treatment of human epidermal growth factor receptor 2 (HER2)-positive breas

190 ctively).Five-year BCSS was highest in human epidermal growth factor receptor 2 (HER2)-positive disea

191 ves clinical outcomes in patients with human epidermal growth factor receptor 2 (HER2)-positive esoph

192 e signatures identifying patients with human epidermal growth factor receptor 2 (HER2)-positive invas

193 pproved for treatment in patients with human epidermal growth factor receptor 2 (HER2)-positive, meta

194 Purpose Human epidermal growth factor receptor 2 (HER2)-positive/hormo

195 y fused a recombinant sialidase to the human epidermal growth factor receptor 2 (HER2)-specific antib

196 imetry of (89)Zr-pertuzumab PET/CT for human epidermal growth factor receptor 2 (HER2)-targeted imagi

197 as to determine whether imaging with a human epidermal growth factor receptor 2 (HER2)-targeted PET t

198 hormone receptor (HR) and negative for human epidermal growth factor receptor 2 (HER2).

199 edict the efficacy of chemotherapy and human epidermal growth factor receptor 2 (HER2, encoded by the

200 e-specific membrane antigen (n = 7) or human epidermal growth factor receptor 2 (n = 5).

201 f breast cancer (luminal A, luminal B, human epidermal growth factor receptor 2 [currently known as E

202 ecular subtypes: luminal A, luminal B, human epidermal growth factor receptor 2 enriched, and basal l

203 which he was eligible on the basis of human epidermal growth factor receptor 2 positivity (>/= 1+ by

204 ogen/progesterone receptor status, and human epidermal growth factor receptor 2 positivity (all P < 0

205 l aptamer-based assay for detection of human epidermal growth factor receptor 2 protein (HER2) cancer

206 egimens based on estrogen receptor and human epidermal growth factor receptor 2 status was also asses

207 try) early breast cancer any nodal and human epidermal growth factor receptor 2 status, were randomly

208 basis of the number of lymph nodes and human epidermal growth factor receptor 2 status.

209 , 1.0 to 1.8) but not among those with human epidermal growth factor receptor 2 subtypes (HR, 1.2; 95

210 n receptor, progesterone receptor, and human epidermal growth factor receptor 2 was found to guide ch

211 ceptor (PR) content, and HER2 content (human epidermal growth factor receptor 2).

212 eptor+, progesterone receptor+, and/or human epidermal growth factor receptor 2+ tumors.

213 eceptor, progesterone receptor, Ki-67, human epidermal growth factor receptor 2, and Elston grade) to

214 ogous cellular immunotherapy targeting human epidermal growth factor receptor 2, for which he was eli

215 well-known estrogen receptor (ER) and human epidermal growth factor receptor 2, the androgen recepto

216 strogen and progesterone receptors and human epidermal growth factor receptor 2, the panel found suff

217 rogesterone receptors and negative for human epidermal growth factor receptor 2, with associated duct

218 vantages in hormone receptor-positive, human epidermal growth factor receptor 2-negative advanced bre

219 B (intermediate and high-risk, locally human epidermal growth factor receptor 2-negative BC).

220 proved IDFS in patients with high-risk human epidermal growth factor receptor 2-negative breast cance

221 Results For 240 human epidermal growth factor receptor 2-negative patients you

222 For 145 human epidermal growth factor receptor 2-negative patients you

223 ry toxicity of trastuzumab therapy for human epidermal growth factor receptor 2-overexpressing (HER2-

224 among breast cancer subtypes, with the human epidermal growth factor receptor 2-positive (HER2+) subt

225 umors (21% v 6%; P = .08), but not for human epidermal growth factor receptor 2-positive (luminal and

226 dard of care for adjuvant treatment of human epidermal growth factor receptor 2-positive breast cance

227 aluated in clinical trials for imaging human epidermal growth factor receptor 2-positive cancer patie

228 r adjuvant treatment of node-positive, human epidermal growth factor receptor 2-positive early-stage

229 esponse to RT, although, in our study, human epidermal growth factor receptor 2-positive tumors seeme

230 s-including hormone receptor-positive, human epidermal growth factor receptor 2-positive, and triple-

231 There was no amplification of the human epidermal growth factor receptor 2/ neu gene.

232 The human epidermal growth factor receptor 3 (HER3) is an interest

233 terized by prominent expression of the human epidermal growth factor receptor 3 (HER3) on the cell su

234 al growth factor receptor 1 (EGFR) and human epidermal growth factor receptor 3 (HER3), leading to pe

235 al growth factor receptor 2 (HER2) and human epidermal growth factor receptor 3 (HER3), was examined.

236 this study, we have shown that the RTK human epidermal growth factor receptor 4 (Her4, also known as

237 Although oncogenic drivers such as epidermal growth factor receptor activation and Phosphat

238 ression of MAN2A1-FER in 4 cell lines led to epidermal growth factor receptor activation of BRAF, MEK

239 d EV release and mitogenic content including epidermal growth factor receptor and c-Src.

240 ted metastasis suppressor interacts with the epidermal growth factor receptor and mediates its downst

241 he VLPs for peptides relevant to cancer from epidermal growth factor receptor and telomerase.

242 hat of wild-type FER, and phosphorylated the epidermal growth factor receptor at tyrosine 88 in its N

243 ced non-small-cell lung cancer (NSCLC) whose epidermal growth factor receptor expression status is po

244 Members of the epidermal growth factor receptor family (ErbB family) po

245 Further, epidermal growth factor receptor I (EGFR)-binding peptid

246 Selective activation of epidermal growth factor receptor in renal proximal tubul

247 Erlotinib is an epidermal growth factor receptor inhibitor approved for

248 Purpuric drug eruptions caused by epidermal growth factor receptor inhibitors are uncommon

249 enter with purpuric skin lesions after using epidermal growth factor receptor inhibitors from January

250 systemic antibiotic treatment; the doses of epidermal growth factor receptor inhibitors were also ch

251 aracterize purpuric skin eruptions caused by epidermal growth factor receptor inhibitors.

252 y rarely been reported in patients receiving epidermal growth factor receptor inhibitors.

253 the FER kinase inhibitor crizotinib and the epidermal growth factor receptor kinase inhibitor canert

254 Parabens and human epidermal growth factor receptor ligand cross-talk in br

255 patients, 8 with and 9 without an activating epidermal growth factor receptor mutation (exon 19 delet

256 arcinoma (NSCLC) patients with an activating epidermal growth factor receptor mutation who were treat

257 pecies partition analysis, we identified the epidermal growth factor receptor on endophilin B1 vesicl

258 Eps15 (epidermal growth factor receptor pathway substrate 15)-h

259 Genes involved in the tumor protein 53 and epidermal growth factor receptor pathways have been exte

260 Inhibition of the epidermal growth factor receptor represents one of the m

261 They regulate epidermal growth factor receptor signalling in Drosophil

262 ol myristate acetate, Gq/11-coupled GPCR, or epidermal growth factor receptor stimulation promotes be

263 (PI3K) mediate the increase independently of epidermal growth factor receptor transactivation.

264 rone receptor (in 54,115 patients) and human epidermal growth factor receptor type 2 (HER2) (in 15,41

265 Previous studies demonstrated that the human epidermal growth factor receptor type 2 (HER2)-targeting

266 d considerable inhibitory percentage against Epidermal Growth Factor Receptor tyrosine kinase (EGFR-T

267 Epidermal growth factor receptor tyrosine kinase inhibit

268 tation, disease progression after first-line epidermal growth factor receptor tyrosine kinase inhibit

269 The epidermal growth factor receptor tyrosine kinase inhibit

270 cell mitogen neuregulin-1 or overexpress the epidermal growth factor receptor validate observations i

271 binding fragments F(ab')2 and Fab) targeting epidermal growth factor receptor were labeled with Alexa

272 of EVT differentiation, the transition from epidermal growth factor receptor(+) villous cytotrophobl

273 us cell line studies that knockdown of EGFR (epidermal growth factor receptor) may be of clinical sig

274 urface receptor on these cells and vesicles (epidermal growth factor receptor, EGFR) reduces the inte

275 ulation of SOCS1 decreased the expression of epidermal growth factor receptor, Ins-Ralpha, and fibrob

276 ifferentiation by forming a complex with the epidermal growth factor receptor, leading to activation

277 ed epitopes on mouse serum albumin and human epidermal growth factor receptor, respectively.

278 and c78(f/+) pancreata leads to reduction of epidermal growth factor receptor, which is critical for

279 The transcriptional regulation of the human epidermal growth factor receptor-2 (HER2) contributes to

280 ptors, including estrogen receptor and human epidermal growth factor receptor-2.

281 bilizing protein cortactin downstream of the epidermal growth factor receptor-Src-Arg kinase cascade

282 inic to select patients who may benefit from epidermal growth factor receptor-targeted therapy in non

283 ere enriched in Dsg2 C-terminal fragment and epidermal growth factor receptor.

284 itated the c-Src-mediated transactivation of epidermal growth factor receptor.

285 64)Cu-/(177)Lu-cetuximab), that acts as anti-epidermal growth factor receptor.

286 mmatory cytokine TNFalpha and ligands of the epidermal growth factor receptor.

287 Following gut epithelial damage, epidermal growth factor receptor/mitogen-activated prote

288 ame extracellular vesicle instead displaying epidermal growth-factor receptor aptamer inhibited ortho

289 terone receptor are not expressed, and human epidermal growth factor-receptor 2 is not amplified or o

290 alterations, are barriers to effective anti-epidermal-growth-factor-receptor (EGFR) therapy.

291 LCN(-/-) cells display slower trafficking of epidermal growth factor receptors (EGFR) from early to l

292 tective antigen, PA) which was redirected to Epidermal Growth Factor Receptors (EGFR) or to human EGF

293 ) and PCA-Tr (also known as delta/notch-like epidermal growth factor-related receptor [DNER]; 0.006%)

294 ion of the ERK pathway in Gnb5(-/-) cells by epidermal growth factor restored M3R-stimulated insulin

295 n activator (LAMTOR) complexes and show that epidermal growth factor stimulation decreases LAMTOR/BOR

296 ant NRAS melanoma, especially in response to epidermal growth factor stimulation.

297 This compound was used to link epidermal growth factor to genome-free MS2 viral capsids

298 agen matrix with and without the presence of epidermal growth factor to probe the intracellular mecha

299 Moreover, SPRY2 increased AKT activation by epidermal growth factor, whereas AKT and also Src inhibi

300 ver and impaired degradation of internalized epidermal growth factor, whereas endosomal recycling pro