ライフサイエンスコーパス: EGF receptor

1 rlotinib, a clinically used inhibitor of the EGF receptor.

2 umor lesions through active targeting of the EGF receptor.

3 verse growth factor receptors, including the EGF receptor.

4 ation of the growth factor receptors Met and EGF receptor.

5 ory role of CD82 in endocytic trafficking of EGF receptor.

6 increased EGF-induced phosphorylation of the EGF receptor.

7 ce and depends on the kinase activity of the EGF receptor.

8 phorylated and associated with the activated EGF receptor.

9 in part through defective regulation of the EGF receptor.

10 the genesis of negative cooperativity in the EGF receptor.

11 ion of the receptor tyrosine kinases MET and EGF receptor.

12 h direct binding and activation of the renal EGF receptor.

13 tive interdomain pocket of the extracellular EGF receptor.

14 B domain of Shc (SHC adaptor protein) to the EGF receptor.

15 ase (RTK) ligands that activate both FGF and EGF receptors.

16 he binding of Grb2 and Shc to the single-Tyr EGF receptors.

17 d signaling via the epidermal growth factor (EGF) receptor.

18 or to an affibody directed against the human EGF receptor 2 (HER2).

19 l Growth Factor Receptors (EGFR) or to human EGF receptors 2 (HER2), which are overexpressed in sever

20 ispecific antibody MCLA-128, targeting human EGF receptors 2 and 3.

21 ates with another kinase, called HER2 (human EGF-receptor 2), we assumed that agents targeting EGFR a

22 nter on invading the uterus increased HLA-G, EGF-Receptor-2, and LIF-Receptor expression on EVT, pres

23 Furthermore, the EGF receptor-3 protein localizes asymmetrically on the c

24 horylated downstream of protein kinase C and EGF receptor activation and is a substrate for protein k

25 rk analysis highlighted the central role for EGF receptor activation in mediating the observed respon

26 imer formation, suggesting that its path for EGF receptor activation involves binding to both monomer

27 H3 and phosphorylates histone H3 at T11 upon EGF receptor activation.

28 ough spatiotemporally regulated responses to EGF receptor activation.

29 tered downstream of epidermal growth factor (EGF) receptor activation, following the phosphorylation

30 ferences in network utilization by different EGF receptor agonists and highlight the need to characte

31 otein/extracellular signal-regulated kinase, EGF receptor and ADAM17 activity.

32 require the tyrosine kinase activity of the EGF receptor and are mediated by complexes containing ac

33 l sulfate and p-cresol sulfate activated the EGF receptor and downstream signaling by enhancing recep

34 racterized the interaction of ErbB3 with the EGF receptor and ErbB2 and assessed the effects of Food

35 ble of compensatory PI3K signaling from both EGF receptor and ErbB2.

36 ch was accompanied by transactivation of the EGF receptor and ERK1/2 phosphorylation.

37 Silencing messenger RNAs and blocking EGF receptor and IL15 antibodies have been used to study

38 samples from patients with CD was reduced by EGF receptor and IL15 blocking antibodies only when used

39 ol sulfate significantly activated the renal EGF receptor and increased the tubulointerstitial expres

40 re an active block to signal transduction by EGF receptor and LIN-12/Notch and have a different mecha

41 other receptor tyrosine kinases such as the EGF receptor and Met.

42 epidermal growth factor (EGF) share the same EGF receptor and previously indistinguishable intracellu

43 eptor tyrosine kinase acts downstream of the EGF receptor and Src tyrosine kinases to promote invadop

44 Mature ECs lack EGF receptors and are refractory to growth signalling.

45 a leads to aberrant activation of TAK1, JNK, EGF receptor, and ERK in distinct microanatomical areas

46 sis in RCE cells was inhibited by CDC or the EGF receptor antagonist AG1478.

47 olonged by new targeting agents such as anti-EGF receptor (anti-EGFR) antibodies.

48 ronectin interactions on the efficacy of the EGF receptor antibody cetuximab, which is used widely fo

49 nd is associated with enhanced and prolonged EGF receptor autophosphorylation.

50 mice administered cetuximab, an inhibitor of EGF receptor binding, and (b) immunological data showing

51 se to certain growth factor receptors (i.e., EGF-receptor but not insulin receptor) and pathogen reco

52 The EGF receptor can bind seven different agonist ligands.

53 uently, we analyzed changes in expression of EGF receptors, cell aspect ratio, and protrusive activit

54 rgement and clustering of endosomes, delayed EGF receptor degradation, and impaired autophagosome mat

55 fficking to LAMP-2-positive compartments and EGF receptor degradation.

56 n of matrix metalloproteinases 2 and 9 in an EGF receptor-dependent manner.

57 a with significantly better survival, and an EGF receptor-deregulated subclass of colon cancers.

58 Activation of the EGF receptors EGFR (ErbB1) and HER2 (ErbB2) drives the p

59 The role of endocytosis in the control of EGF receptor (EGFR) activation and cell signaling was ex

60 Simultaneous activation of the EGF receptor (EGFR) and a thrombin receptor (protease-ac

61 ity was accompanied by reduced expression of EGF receptor (EGFR) and an increased degradation rate of

62 geting of prominent cancer antigens, such as EGF receptor (EGFR) and c-MET, by bsAbs has raised incre

63 ion of its chloride-channel activity reduced EGF receptor (EGFR) and calmodulin-dependent protein kin

64 Here, we show that the EGF receptor (EGFR) and HER2 function cooperatively to i

65 phosphorylation of specific tyrosines in the EGF receptor (EGFR) and in inefficient activation of the

66 Here, we report that the oncogenic EGF receptor (EGFR) and its inhibitors reprogram phospho

67 EGF receptor (EGFR) and MET (the receptor tyrosine kinas

68 Hyperactive EGF receptor (EGFR) and mutant p53 are common genetic ab

69 n that MUC1-C, in turn, forms complexes with EGF receptor (EGFR) and promotes EGFR-mediated activatio

70 racellular domain of NRP1 interacts with the EGF receptor (EGFR) and promotes its signaling cascade e

71 In glioblastoma (GBM), the EGF receptor (EGFR) and Src family kinases (SFKs) contri

72 ed by temporal compensatory increases in the EGF receptor (EGFR) and the hepatocyte growth factor rec

73 odimeric IgG derived from anti-HER2 and anti-EGF receptor (EGFR) antibody was shown to induce a highe

74 sine kinase inhibitors (TKI) that target the EGF receptor (EGFR) are effective in most non-small cell

75 I-1757 inhibits STAT3 dimerization and STAT3-EGF receptor (EGFR) binding in intact cells.

76 ternalization and partial degradation of the EGF receptor (EGFR) by the endo-lysosomal pathway.

77 nctions as a tumor suppressor that restricts EGF receptor (EGFR) cell surface occupancy as well as Ak

78 udy a mechanism by which dimerization of the EGF receptor (EGFR) cytoplasmic domain is transmitted to

79 tive late endosomes and lysosomes and slowed EGF receptor (EGFR) degradation.

80 Stress exposure triggers ligand-independent EGF receptor (EGFR) endocytosis, but its post-endocytic

81 sponse to LPS is impaired by down regulating EGF receptor (EGFR) expression or by using the EGFR inhi

82 Because TNBC commonly displays EGF receptor (EGFR) expression, and combinations of mono

83 The EGF receptor (EGFR) family comprises four homologs in hu

84 ErbB3 (HER3) is a member of the EGF receptor (EGFR) family of receptor tyrosine kinases,

85 en by signature genetic alterations, such as EGF receptor (EGFR) gene amplification and mutation, pla

86 ive with amplification and expression of the EGF receptor (EGFR) gene.

87 Tyrosine kinase inhibitors (TKIs) of the EGF receptor (EGFR) have provided a significant improvem

88 The EGF receptor (EGFR) HER3 is emerging as an attractive ca

89 e ligands on subunit-subunit interactions in EGF receptor (EGFR) homodimers and EGFR/ErbB2 heterodime

90 s barrier function by transactivation of the EGF receptor (EGFR) in intestinal epithelial cells.

91 dying enterocyte triggers activation of the EGF receptor (Egfr) in stem cells within a discrete radi

92 EGF receptor (EGFR) inhibition is efficacious in cancer

93 We therefore examined the effects of the EGF receptor (EGFR) inhibitor erlotinib on liver fibroge

94 Because oncogene MET and EGF receptor (EGFR) inhibitors are in clinical developme

95 ening assay prompted us to determine whether EGF receptor (EGFR) inhibitors stimulate AQP2 traffickin

96 ficient to heighten therapeutic responses to EGF receptor (EGFR) inhibitors.

97 role in the trafficking of the ligand-bound EGF receptor (EGFR) internalized through receptor-mediat

98 In this study we show that EGF receptor (EGFR) is activated following pemphigus vul

99 The EGF receptor (EGFR) is amplified and mutated in glioblas

100 dermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell mig

101 Ligand-induced ubiquitylation of EGF receptor (EGFR) is an important regulatory mechanism

102 Overexpression of the EGF receptor (EGFR) is recognized as a widespread oncoge

103 The kinase activity of the EGF receptor (EGFR) is required, because the potent and

104 ously established that overexpression of the EGF receptor (EGFR) is sufficient to induce tumor format

105 The clinical efficacy of EGF receptor (EGFR) kinase inhibitors gefitinib and erlo

106 lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term wi

107 n-induced type 1 diabetes, podocyte-specific EGF receptor (EGFR) knockout mice (EGFR(podKO)) and thei

108 EGF receptor (EGFR) ligand and species specificities of

109 elevance of iRhom2 in regulating shedding of EGF receptor (EGFR) ligands is established by a lack of

110 or (EGF), leading to decreased activation of EGF receptor (EGFR) on target cells and, eventually, dam

111 Signaling by the EGF receptor (EGFR) or cAMP amplified the activation of

112 Activation of the EGF receptor (EGFR) or the Hippo signaling pathway can c

113 EGF receptor (EGFR) promotes tumor growth as well as rad

114 at phosphorylation of PCNA at Tyr-211 by the EGF receptor (EGFR) protects PCNA from polyubiquitylatio

115 ect targets of miR-148a were identified, the EGF receptor (EGFR) regulator MIG6 and the apoptosis reg

116 face pro-EGF to HMW-EGF that stimulated HeLa EGF receptor (EGFR) reporter cells and EGFR-dependent tu

117 tumors harboring activating mutations in the EGF receptor (EGFR) show good initial treatment response

118 the role of the Tid1 isoforms in regulating EGF receptor (EGFR) signaling and lung cancer progressio

119 disintegrin and metalloprotease 17) controls EGF receptor (EGFR) signaling by liberating EGFR ligands

120 n of S. aureus, activates TNF receptor 1 and EGF receptor (EGFR) signaling cascades that can perturb

121 ay dependence or (ii) constitutive autocrine EGF receptor (EGFR) signaling driven by c-Jun-mediated E

122 evels of functional proteins associated with EGF receptor (EGFR) signaling in pairs of U87EGFR varian

123 Enhanced EGF receptor (EGFR) signaling is a hallmark of many huma

124 Despite extensive study of the EGF receptor (EGFR) signaling network, the immediate pos

125 The importance of the EGF receptor (EGFR) signaling pathway in the development

126 Activated EGF receptor (EGFR) signaling plays an instrumental role

127 ential for the termination of EGF-stimulated EGF receptor (EGFR) signaling.

128 ype 1 matrix metalloproteinase (MT1-MMP) and EGF receptor (EGFR) to the cell surface during invadopod

129 Immunofluorescence showed altered EGF receptor (EGFR) trafficking, where EGFR remained mem

130 eta1-adrenergic receptor stimulation-induced EGF receptor (EGFR) transactivation in addition to Gbeta

131 Activation of EGF receptor (EGFR) triggers signaling pathways regulati

132 Acquired resistance to EGF receptor (EGFR) tyrosine kinase inhibitors (TKIs) is

133 EGF-induced EGF receptor (EGFR) tyrosine phosphorylation and extrace

134 We found that EGF receptor (EGFR) was highly active in the TRAIL-resis

135 owth factor receptor-cytohesin interactions, EGF receptor (EGFR) was investigated in induced MEFs.

136 or-activated receptor, because inhibition of EGF receptor (EGFR) with cetuximab or EGF-depleted amnio

137 diated enhanced HCV entry and endocytosis of EGF receptor (EGFR), an HCV entry cofactor and erlotinib

138 teracts with a variety of kinases (PKC, FES, EGF receptor (EGFR), and JAK3) that are activated by it,

139 SCs from wild-type mice expressed functional EGF receptor (EGFR), and systemic administration of EGF

140 Anaplastic lymphoma kinase (ALK), EGF receptor (EGFR), and V-Ki-ras2 Kirsten rat sarcoma v

141 imulates TGFbeta signaling and activates the EGF receptor (EGFR), but the relative contribution of th

142 le receptor-tyrosine kinases (RTKs), such as EGF receptor (EGFR), ErbB-2, FGF receptor (FGFR), and ma

143 r (EGF)-like ligand that signals through the EGF receptor (EGFR), in both osteoblasts and osteocytes.

144 like growth factor (HB-EGF), a ligand of the EGF receptor (EGFR), in nutrient-induced beta-cell proli

145 se tumors harbor activating mutations in the EGF receptor (EGFR), increased responses to platinum-bas

146 ke growth factor (HBEGF) is a ligand for the EGF receptor (EGFR), one of the most commonly amplified

147 Although both CC and SC expressed EGF receptor (EGFR), the EGFR-neutralizing monoclonal an

148 (HGF)/MET and epidermal growth factor (EGF)/EGF receptor (EGFR), two key signal transduction systems

149 ein (Vn) is a neuregulin-like ligand for the EGF receptor (Egfr), which is necessary for global devel

150 first six amino acids of this segment of the EGF receptor (EGFR), which lies in close association wit

151 cers is correlated with higher expression of EGF receptor (EGFR), whose overexpression and/or mutatio

152 The EGF receptor (EGFR)-directed monoclonal antibody cetuxim

153 (UTMD) could be used to enhance delivery of EGF receptor (EGFR)-directed siRNA to murine squamous ce

154 Many feedback loops are present in the EGF receptor (EGFR)-ERK network, but the mechanisms driv

155 e through modification of BC function via an EGF receptor (EGFR)-mediated mechanism.

156 and neck (HNSCC) overexpress ERBB1/EGFR, but EGF receptor (EGFR)-targeted therapies have yielded disa

157 ion as a mechanism of acquired resistance to EGF receptor (EGFR)-targeted therapies in non-small cell

158 ndent on the tyrosine kinase activity of the EGF receptor (EGFR).

159 e use luciferase fragment complementation in EGF receptor (EGFR)/ErbB2 heterodimers to probe the mech

160 the autocrine or paracrine activation of the EGF receptor (EGFR)/mitogen-activated protein/extracellu

161 ment by crawling depends on signaling by the EGF receptor (EGFR); however, this was not required for

162 CERT determines the signaling output of the EGF receptor (EGFR/ErbB1), which is upregulated in appro

163 ErbB family members, such as ErbB2 (HER2) or EGF receptor (EGFR; HER1), enhancing phosphorylation of

164 Blockade of EGF receptors (EGFR) causes cell death.

165 trigger the release of ligands that activate EGF receptors (EGFR) on the granulosa, thereby initiatin

166 degradation of the epidermal growth factor (EGF) receptor (EGFR) after its activation and internaliz

167 Epidermal growth factor (EGF) receptor (EGFR) has been implicated in tumor develo

168 ain shedding of the epidermal growth factor (EGF) receptor (EGFR) ligand heparin-binding EGF-like gro

169 aling proteins with epidermal growth factor (EGF) receptors (EGFR) using biotinylated EGF bound to st

170 s the expression of epidermal growth factor (EGF) receptors (EGFR, ERBB3) and production of EGF-like

171 ed in testes from animals with soma-depleted EGF-Receptor (EGFR).

172 ciated pool colocalizes with transferrin and EGF receptors (EGFRs) and early endosome antigen 1, but

173 In MDA-MB-468 cells, cell surface EGF receptors (EGFRs) promote cell growth, whereas intra

174 ifference in the rates of degradation of the EGF receptor (ErbB1) and ErbB2 upon treatment of cells w

175 ur study also shows that all pairings of the EGF receptor, ErbB2, and ErbB3 form ligand-independent d

176 n of several tumor-enhancing RTKs, including EGF receptor, ErbB2, hepatocyte growth factor receptor (

177 GPER-mediated signaling, which involved the EGF receptor/ERK/c-Fos/AP1 transduction pathway, as asce

178 EGF activated the EGF receptor/ERK/p90RSK and Rho/Rho kinase signaling pat

179 tidic acid increased phosphorylation of AKT, EGF receptor, ERK1/2, JNK1/2/3, and c-Jun.

180 eceptor, they bound poorly to the single-Tyr EGF receptors, even those that bound full-length Grb2 an

181 rotein (GFP)-tagged epidermal growth factor (EGF) receptor expressed in Jurkat cells with immobilized

182 HER-2 is a member of the EGF receptor family and is overexpressed in 20-30% of br

183 ly approved targeted inhibitors of the human EGF receptor family.

184 d expression of the epidermal growth factor (EGF) receptor family member ErbB3 (HER3).

185 planation for the apparent preference of the EGF receptor for dimerizing with ErbB2 and suggest that

186 also releases other Cbl targets, such as the EGF receptor, from Cbl-mediated signal attenuation.

187 In many GBMs, the EGF receptor gene (EGFR) is amplified and may be truncat

188 Accordingly, reduction in the levels of the EGF receptor gene contributes to the activation of Esrrb

189 The EGF receptor has seven different cognate ligands.

190 Aberrant expression of EGF receptors has been associated with hormone-refractor

191 The human EGF receptor (HER/EGFR) family of receptor tyrosine kina

192 R2 heterodimerizes with other members of the EGF receptor/HER/ErbB family, and the HER2-HER3 dimer fo

193 is study provides valuable insights into the EGF receptor/HER/ErbB kinase structure and interactions,

194 EGF receptor/IL15R-alpha cooperation regulates intestina

195 promoted association of Src and AR with the EGF receptor in response to EGF treatment and enhanced t

196 increased plasma membrane expression of the EGF receptor in resting cells and increased EGF-induced

197 wth factor (EGF)-dependent activation of the EGF receptor in the ALA neuron.

198 also performed to estimate the expression of EGF receptors in healed corneal tissue.

199 racer (18)F-IRS for molecular imaging mutant EGF Receptors in vitro and vivo.

200 Epidermal growth factor (EGF) receptor in HUVECs was LeY modified.

201 detect upregulated epidermal growth factor (EGF) receptor in orthotopic pancreatic xenografts using

202 tivation by mutant TRPC6, a cell-autonomous, EGF receptor-independent mechanism and a non-cell-autono

203 e signaling capabilities of these single-Tyr EGF receptors indicated that they can activate a range o

204 s lysosomal targeting and degradation of the EGF receptor, indicating that it targets host-membrane t

205 cell survival and proliferation, and active EGF receptor-induced brain tumorigenesis.

206 However, treatment of GCs with the EGF receptor inhibitor AG1478, a dominant-negative RAS,

207 genous AMF overcame the inhibitory effect of EGF receptor inhibitor gefitinib on invasive motility by

208 In addition, treatment with EGF receptor inhibitors reduced retinal vascular leakage

209 olorectal cancer or in patients resistant to EGF receptor inhibitors.

210 n of downstream effector pathways shows that EGF receptor inhibits the Hippo pathway through activati

211 The EGF receptor is a classic receptor tyrosine kinase.

212 If the EGF receptor is kinase active, this results in the phosp

213 The epidermal growth factor (EGF) receptor is a member of the ErbB family of receptor

214 mainly known as a negative regulator of the EGF receptor, is an important mediator of progesterone s

215 ated in the spatiotemporal regulation of the EGF receptor, is required for TRAIL-induced cell death i

216 tors, including the epidermal growth factor (EGF) receptor, is key to various cellular processes, suc

217 surface precursor of an alternately spliced EGF receptor isoform and that sEGFR binds to EGF with hi

218 However, if the EGF receptor kinase is kinase dead, the ErbB2 kinase is

219 appaB activated by oncogenes such as Ras and EGF receptor leads to cell-autonomous effects, abrogatin

220 Depletion of Mtss1 results in decreased EGF receptor levels and decreased phosphorylation of Erk

221 Late posttransplant EGF and EGF receptor levels were reduced with erlotinib.

222 presence of a midline signal provided by the EGF receptor ligand Spitz.

223 m knockdown results in overexpression of the EGF receptor ligand vein (vn), which further activates E

224 talloprotease-mediated release of a presumed EGF receptor ligand.

225 erting enzyme, is the major sheddase for the EGF receptor ligands and is considered to be one of the

226 different growth factors suggests that these EGF receptor ligands fall into two major groups as follo

227 ferences in biological response to different EGF receptor ligands may result from partial agonism for

228 lar peptides (C-type natriuretic peptide and EGF receptor ligands) maintain the low level of cGMP in

229 EGF receptor ligands, which activate Rac, can promote th

230 he EGF receptor when stimulated by the seven EGF receptor ligands.

231 BTC acts via both the EGF receptor, located on NSCs, and ErbB4, located on neu

232 lves NF-kappaB-dependent IL-8 expression and EGF receptor-mediated MAPK activation in human colonocyt

233 y and which tyrosines are required to enable EGF receptor-mediated signaling, we generated a series o

234 ein-protein interactions associated with the EGF-receptor-mediated PI3K signaling pathway.

235 N-glycans restricts epidermal growth factor (EGF) receptor mobility in the plasma membrane and acts s

236 LaS3 cell lines, as well as H1975 activating-EGF receptor mutant lung cancer cell resulted in dephosp

237 zed the binding of (125)I-EGF to a series of EGF receptor mutants in the intracellular juxtamembrane

238 lation is dependent on PDK1 and PI3K but not EGF receptor or IGF1R.

239 ta subunits was blocked by inhibition of the EGF receptor or STAT3 but not by the PI3K/AKT or MEK/ERK

240 nes were linked to the Wnt, Hippo, TGF-beta, EGF receptor, or PI3K pathways, all involved in colorect

241 o enhanced cetuximab-mediated recruitment to EGF receptor-overexpressing cancer cells.

242 Accordingly, blockade of the EGF receptor partially abrogated Dkk1-mediated hematopoi

243 nt advances in our understanding of the AREG-EGF receptor pathway and its involvement in infection an

244 is revealed that the presence of a synthetic EGF receptor peptide significantly decreased the spectro

245 t also elicited prosurvival signaling via an EGF receptor/phosphoinositide 3-kinase (PI3K) pathway.

246 ation tissue area, vascularity, and IGF1 and EGF receptor phosphorylation are increased in GM3S SNA-t

247 ransferrin from endosomes, or degradation of EGF receptor proceeds unperturbed in cells with impaired

248 ith deep-seated gliomas that overexpress the EGF receptor produced an estimate of available receptor

249 rbital, which is not a CAR ligand, binds the EGF receptor, reversing the EGF signal to monomerize CAR

250 s "checkpoint." Dysregulated CME also alters EGF receptor signaling and leads to constitutive activat

251 Suppression of EGF receptor signaling appeared necessary for the therap

252 breast cancer, emphasizing the importance of EGF receptor signaling in breast tumor pathogenesis and

253 proliferative activities along with enhanced EGF receptor signaling in the articular cartilage and in

254 Here, we show that EGF receptor signaling is required to maintain the proli

255 NEU3 up-regulation stimulates the EGF receptor signaling pathway, which in turn activates

256 promotes growth by regulating the Hippo and EGF receptor signaling pathways.

257 beta cells but also release EGF to activate EGF receptor signaling that inhibits TGFbeta1-activated

258 ed for SREBP-1 activation by angiotensin II, EGF receptor signaling was necessary for activation of t

259 rTMD1 inhibited EGF receptor signaling, chemotaxis, and tube formation i

260 reased expression of gene pathways mediating EGF receptor signaling, circadian exercise, striated mus

261 gulated kinases 1 and 2 (MEK/ERK1/2) and (b) EGF receptor signaling.

262 gene within bract cells of the pupal leg by EGF receptor signaling.

263 e F-BAR protein PACSIN2 in the regulation of EGF receptor signaling.

264 e cross-talk through indirect enhancement of EGF receptor signaling.

265 nctions to cause Dll to become responsive to EGF receptor signaling.

266 mesenchyme proliferation by sustaining Hbegf-EGF receptor signaling.

267 to drugs that block epidermal growth factor (EGF) receptor signaling could be caused by aberrant acti

268 n-regulated nuclear epidermal growth factor (EGF) receptor signaling in the CySC lineage is essential

269 ntially involved in epidermal growth factor (EGF) receptor signaling.

270 etalloprotease 17), a principal regulator of EGF-receptor signaling and TNFalpha release, is rapidly

271 or ligand vein (vn), which further activates EGF receptor signalling and integrin expression non-cell

272 inly the JAK/STAT signalling pathway and the EGF receptor signalling pathway.

273 een of signaling molecules, we identified an EGF receptor (Smed-EGFR-5) as a crucial regulator of bra

274 Kaiso to the nucleus that is reversed by the EGF receptor-specific kinase inhibitor, PD153035.

275 epithelial invasion by derepressing upstream EGF receptor, SRC tyrosine kinase, and phosphoinositide

276 Our findings reveal a novel link between EGF receptor stimulation, ILK-containing complexes, and

277 signaling via both the TGFbeta-receptor and EGF receptor suggesting that PAR2 utilizes transactivati

278 e F-BAR-domain protein PACSIN2 in regulating EGF receptor surface levels and EGF-induced downstream s

279 For example, resistance to EGF receptor targeting occurs commonly, more so than was

280 mediated signaling, we generated a series of EGF receptors that contained only one tyrosine in their

281 lization at the plasma membrane of CD44, the EGF receptor, the ABCB1 and ABCG2 drug transporters, and

282 eting signaling via MET and CD44 during anti-EGF receptor therapy of patients with colorectal cancer

283 adapter proteins bound readily to wild-type EGF receptor, they bound poorly to the single-Tyr EGF re

284 aling axis is inhibited, the transit time of EGF receptor through early endosomes are accelerated, mi

285 r a MAPK signaling cascade downstream of the EGF receptor to investigate how interlinked positive and

286 gether, our studies reveal a crucial link of EGF receptor to NF-kappaB activation and tumor progressi

287 localization of the epidermal growth factor (EGF) receptor to the plasma membrane, prolonging EGF sig

288 1-dependent adaptive CME selectively altered EGF receptor trafficking, enhanced cell migration in vit

289 ents autocrine ligand shedding and resultant EGF receptor transactivation, it also leads to an accumu

290 internalized EGF as well as the (activated) EGF receptor translocated to PACSIN2-positive endosomes.

291 further found that epidermal growth factor (EGF) receptor up-regulates Kaiso at the RNA and protein

292 s to cell surface antigens including MET and EGF receptor, we have experimentally validated our model

293 Signals received via the EGF Receptor were necessary for the transience in Yan no

294 rb2, PI3K, p52 Shc, p66 Shc, and Shp2 to the EGF receptor when stimulated by the seven EGF receptor l

295 trikingly different from those of 5HT-2C and EGF receptors, which demonstrate the usefulness of the b

296 but require back-to-back dimerization of the EGF receptor with ErbB2.

297 binding to quantitate the interaction of the EGF receptor with ErbB2.

298 mulation was caused by marked endocytosis of EGF receptors with concomitant ERK attenuation, which st

299 activates non-receptor tyrosine kinases and EGF receptor, with a Src family kinase as a required int

300 veolae, leading to increased dimerization of EGF receptor within the confined surface area of caveola