ライフサイエンスコーパス: EGF

1 EGF stimulation resulted in fast but transient activatio

2 co-immunoprecipitation with thrombospondin-4-EGF domain.

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

4 ons in which oxidation decreased upon adding EGF fall along the dimerization interface, consistent wi

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

6 1-dependent adaptive CME selectively altered EGF receptor trafficking, enhanced cell migration in vit

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

8 Although EGF:EGFR complexes were rapidly accumulated in endosomes

9 om Cic conditional knockout mice bypassed an EGF requirement for proliferation and displayed a defect

10 ced organoid growth efficiency ex vivo in an EGF-dependent manner.

11 ases the expression of Matrilin2 (MATN2), an EGF-like domain-containing protein that traps EGFR at th

12 tor SB431542 together with ascorbic acid and EGF were required to promote hiPSCs-BAP differentiation

13 tional transactivation of PDGFRA by EGFR and EGF-induced receptor heterodimerization, both of which a

14 ceptors and the tyrosine kinase with IgG and EGF domains-2 (Tie2) receptor by angiopoietins is requir

15 rosine kinase family with immunoglobulin and EGF homology domains, are receptor tyrosine kinases foun

16 tyrosine kinase with immunoglobulinlike and EGF-like domains 1/angiopoietin-1, p21-activated kinase,

17 re we report the structure of the lectin and EGF domains of L-selectin bound to a fucose mimetic; tha

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

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

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

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

22 two different cell lines, that in serum- and EGF-free conditions, EGFR or HER2 activity increase spre

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

24 teins in response to growth factors, such as EGF, using a short C-terminal motif.

25 wable and forbidden cell-fate transitions as EGF or Notch levels change, and explains surprising obse

26 condary factors, such as membrane-associated EGF-CFC family proteins.

27 er pathways, such as nuclear factor kappa B, EGF, Wnt, and B-cell lymphoma 2.

28 Because EGF can strongly bind EGFR, which is overexpressed in ca

29 ead to strong epistatic interactions between EGF and Notch.

30 secreted factor collagen and calcium binding EGF domains 1 (CCBE1) in this process.

31 extended central array of 11 calcium-binding EGF domains and flexible TGFbeta-binding C-terminus.

32 s of implantation, including Heparin binding EGF-like growth factor and Mucin 1, exhibit expression a

33 increased the expression of heparin-binding EGF-like growth factor (HB-EGF) and activin AB in LTBI s

34 GFR ligands amphiregulin and heparin-binding EGF-like growth factor (HB-EGF) are upregulated, and exo

35 oblast growth factor (FGF2), heparin-binding EGF-like growth factor (HBEGF), vascular endothelial gro

36 ssing the EGFR ligand, human heparin-binding EGF-like growth factor (hHB-EGF), in renal proximal tubu

37 tivation of the EGFR-ERK pathway by blocking EGF-mediated EGFR dimerization and internalization but a

38 pSMAD2, bone morphogenetic protein 4 (BMP4), EGF, or PDGF was unaffected by the TAT-SNX9 peptide.

39 Although both EGF treatments increased collective sheet displacement a

40 growth factor C (VEGFC), betacellulin (BTC), EGF, epiregulin (EREG), and other members of the transfo

41 ge chemotaxis, while activation of ERK1/2 by EGF alone did not inhibit fMLF-mediated migration of HEK

42 cell surface to facilitate its activation by EGF.

43 choices are displayed in a plane defined by EGF and Notch signaling levels.

44 he induction of Snail and Slug expression by EGF, and this effect was associated with increased EGFR

45 in c-Fos protein which cannot be induced by EGF or accumulates constitutively and lead to decreased

46 lying the precise regulation of NF-kappaB by EGF, and highlight the critical role of nuclear MIIP in

47 Stimulation by EGF does not appear to induce a change in the density of

48 nd C2 domain containing 1), CELSR3 (Cadherin EGF LAG seven-pass G-type receptor 3), NIPBL (Nipped-B-l

49 control of initiation and assembly of CCPs, EGF stimulation also elicited a Ca(2+)- and PKC-dependen

50 ERK1&2 kinase activities reveals concomitant EGF-mediated activations of both kinases in HeLa cells.

51 ces of receptor-bound fluorophore-conjugated EGF ligands.

52 hCDC14A counteracts EGF-induced rearrangements of actin cytoskeleton by deph

53 nt of human breast cancer cells with CXCL12, EGF and HRG, and HMEC-CXCR2 cells with CXCL8 facilitated

54 (177)Lu-DOTA-trastuzumab Fab or (177)Lu-DOTA-EGF.

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

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

57 romote the malignant phenotype via enhancing EGF-mediated mesenchymal phenotype.

58 Exogenous EGF increased S100A4 mRNA levels in 231BR-EGFP cells (1.

59 ion in response to high glucose or exogenous EGF.

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

61 ic cell fate decisions, has 36 extracellular EGF domains that are glycosylated in variable and comple

62 N9 targets the extracellular EGF-like repeats (ELR) 11-13 in Notch1, and therefore se

63 Epidermal growth factor (EGF) and insulin receptor tyrosine kinases (RTKs) exempl

64 , which can mediate epidermal growth factor (EGF) and neuregulin signalling in multiple tissues, is u

65 de as controls, and epidermal growth factor (EGF) as a physiologically-relevant influencer of cell me

66 al association with epidermal growth factor (EGF) but not transferrin (Tf) trafficking pathways as sh

67 at at physiological epidermal growth factor (EGF) concentrations, EGFR assembles into oligomers, as i

68 ectional sensing of epidermal growth factor (EGF) gradients and invasive 3D migration of breast cance

69 ation of cells with epidermal growth factor (EGF) induces internalization and partial degradation of

70 wo-color imaging of epidermal growth factor (EGF) ligand and clathrin revealed the dynamics of EGF-ac

71 in response to the epidermal growth factor (EGF) ligand, while also inhibiting formation of the EGFR

72 ways, including the epidermal growth factor (EGF) pathway.

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

74 t with Dkk1 induced epidermal growth factor (EGF) secretion.

75 pha (TGF-alpha) and epidermal growth factor (EGF) share the same EGF receptor and previously indistin

76 a central role for epidermal growth factor (EGF) signaling during in vivo neoblast expansion mediate

77 nd predominantly on epidermal growth factor (EGF) signaling, and to a lesser extent, on aberrant Wnt-

78 so demonstrate that epidermal growth factor (EGF) stabilizes PD-L1 via GSK3beta inactivation in basal

79 Following epidermal growth factor (EGF) stimulation, activated ERK1/2 is recruited to immed

80 Epidermal growth factor (EGF) was found to stimulate CAR homodimerization, thus c

81 duces sleep through epidermal growth factor (EGF)-dependent activation of the EGF receptor in the ALA

82 involving enhanced epidermal growth factor (EGF)-dependent Akt/GSK3beta phosphorylation.

83 s binding to F-box, epidermal growth factor (EGF)-induced c-Fos S374 phosphorylation dissociates c-Fo

84 highly constrained epidermal growth factor (EGF)-like domains of Pfs25 block sexual-stage developmen

85 Heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF) is a ligand for the EGF

86 T3 was critical for epidermal growth factor (EGF)-stimulated cell transformation of the HaCaT immorta

87 ased invadopodia in epidermal growth factor (EGF)-stimulated cells.

88 alization, inhibits epidermal growth factor (EGF)-stimulated Ras signaling and diminishes tumorigenes

89 ifferentiation cue, epidermal growth factor (EGF).

90 beta (TGFbeta) and epithelial growth factor (EGF).

91 owth factors of the epidermal growth factor (EGF)/neuregulin family are involved in tumor progression

92 lls stimulated with epidermal growth factor (EGF): 1) phospho-specific mass spectrometry; 2) far-West

93 ting levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 liga

94 agent doxorubicin (DXR) and growth factors (EGF and IGF-1).

95 etion of mitogenic epidermal growth factors (EGFs) by repressing transcription of the EGF maturation

96 First, EGF-mediated activation of EGFR blunted fusion kinase in

97 ata show that EGFR recruits TMEM43 following EGF stimulation.

98 tial positioning of RTKs in target cells for EGF and insulin action, the temporal extent of signaling

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

100 endymoma cell lines created by selection for EGF/FGF2-independent proliferation exhibited constitutiv

101 Milk fat globule-EGF factor 8 (MFG-E8) maintains the intestinal homeostas

102 e analyze 20 signaling proteins during a 1-h EGF stimulation time course using a panel of 35 antibodi

103 phalus; however, the relationship between HB-EGF and hydrocephalus is unclear.

104 induces decidualization via the canonical HB-EGF and COX-2 pathways.

105 creased Chi3l1-stimulated epithelial cell HB-EGF production and macrophage MAPK/Erk and PKB/Akt activ

106 athophysiological mechanism that elevated HB-EGF can elicit VEGF induction and hydrocephalus.

107 Our results support the idea that excess HB-EGF leads to a significant elevation of VEGF and ventric

108 f heparin-binding EGF-like growth factor (HB-EGF) and activin AB in LTBI samples.

109 d heparin-binding EGF-like growth factor (HB-EGF) are upregulated, and exogenous addition of these li

110 idermal growth factor-like growth factor (HB-EGF) is an angiogenic factor mediating radial migration

111 We show that mice overexpressing human HB-EGF with beta-galactosidase reporter exhibit an elevated

112 uces decidualization via up-regulation of HB-EGF and COX-2.

113 autotaxin (ATX) in pregnant mice leads to HB-EGF and COX-2 down-regulation near embryos and attenuate

114 ancy, up-regulation of heparin-binding (HB-) EGF and cyclooxygenase-2 (COX-2) in the uterine epitheli

115 mesenchyme proliferation by sustaining Hbegf-EGF receptor signaling.

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

117 hHB-EGF expression increased tyrosine kinase phosphorylation

118 heparin-binding EGF-like growth factor (hHB-EGF), in renal proximal tubule epithelium.

119 atelets released high-molecular-weight (HMW)-EGF, produced by a single cleavage between the EGF and t

120 hrombin-, or collagen-induced release of HMW-EGF.

121 EC1, which hydrolyzes pro-EGF to soluble HMW-EGF, that HMW-EGF is active, that proteolytic cleavage o

122 rolyzes pro-EGF to soluble HMW-EGF, that HMW-EGF is active, that proteolytic cleavage of pro-EGF firs

123 d ADAMDEC1 hydrolyzed surface pro-EGF to HMW-EGF that stimulated HeLa EGF receptor (EGFR) reporter ce

124 e sole source of EGF in circulation, yet how EGF is stored or released from stimulated cells is undef

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

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

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

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

129 sphorylated ERK1/2, and cells on immobilized EGF exhibited higher pPLCgamma1, which was localized at

130 icantly decreased persistence on immobilized EGF.

131 ined, these results suggest that immobilized EGF increases collective keratinocyte displacement via a

132 mained membrane-localized in the immobilized EGF condition.

133 l speed, only cells treated with immobilized EGF exhibited directed migration, as well as 2-fold grea

134 ur study reveals a novel function of CDK2 in EGF-induced cell transformation and the associated signa

135 e glycans cooperatively stabilize individual EGF repeats through intramolecular interactions, thereby

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

137 t triggering allostery that opens the lectin/EGF domain hinge.

138 gers further allostery that opens the lectin/EGF domain hinge.

139 plied to a biological problem, i.e., ligand (EGF) induced changes in the conformation of the external

140 We profile two such genes, Delta/Notch-like EGF repeat containing (Dner) and nuclear factor I/A (Nfi

141 ions on Notch1 epidermal growth factor-like (EGF) domains 8 and 12 engage the EGF3 and C2 domains of

142 Epidermal growth factor-like (EGF) repeats are also small cysteine-rich protein motifs

143 se residues on epidermal growth factor-like (EGF) repeats of Notch.

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

145 ned effects of HC-HA/PTX3 on cell migration (EGF + FGF-2 + TGF-beta1) and collagen gel contraction (T

146 Moreover, EGF secreted by TAMs activated EGFR on tumor cells, whic

147 d receptors are not required to support most EGF-stimulated signaling but identify Tyr-992 and its bi

148 let MPs (CD31(+)CD41(+)MPs), eosinophil MPs (EGF-like module-containing mucin-like hormone receptor-l

149 Multiple EGF-like domains 10 (Megf10) is a class F scavenger rece

150 Multiple EGF-like domains 10 (Megf10) is emerging as an essential

151 POFUT1 modify the Notch receptor on multiple EGF repeats and are essential for full Notch function.

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

153 n soft surfaces, neither EGFR inhibition nor EGF stimulation have any effect on cell motility.

154 que downstream effector of TGF-alpha but not EGF signaling via threonine 308-phosphorylated Akt.

155 Of note, EGF signaling weakened the interaction of CAR DBD T38D w

156 the roles of EGFR and HER2 in the absence of EGF both for normal and cancerous growth.

157 Cellular activities of EGF-CFC proteins have been described, but their molecula

158 Addition of EGF at that point increases spreading and contractions,

159 eased softness and decreased adhesiveness of EGF-stimulated cancer cells, implicating acquisition of

160 However, deduction of EGF-activated pathways from TGFalpha-activated pathways

161 ligand and clathrin revealed the dynamics of EGF-activated clathrin-mediated endocytosis during inter

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

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

164 Restored TG1 expression of EGF-stimulated differentiated Adam17(-/-) keratinocytes

165 in a quality control pathway for folding of EGF repeats in proteins such as Notch.

166 P release reverses the transient increase of EGF-mediated ERK1&2 kinase activity while reinforcing PK

167 Inhibition of EGF signalling by gefitinib destabilizes PD-L1, enhances

168 m cell quiescence by selective inhibition of EGF/MAPK signaling and define culture conditions that di

169 4, which signal downstream after ligation of EGF, and which show aberrant expression in several other

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

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

172 Platelets are the sole source of EGF in circulation, yet how EGF is stored or released fr

173 line, was found to be the dominant source of EGF patterning activity.

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

175 7)Lu- and (111)In-labeled trastuzumab Fab or EGF killed tumor cells that predominantly expressed HER2

176 77)Lu- or (111)In-labeled trastuzumab Fab or EGF.

177 id cultures from ISCs stimulated with HGF or EGF and assessed intestinal differentiation by immunohis

178 noma organoid expansion stimulated by HGF or EGF using adenomas derived from Lgr5(Creert2)/Met(fl/fl)

179 om crypts and adenomas, stimulated by HGF or EGF, that were derived from mice expressing different CD

180 2-O-tetradecanoylphorbol-13-acetate (TPA) or EGF in human prostate cancer (PCa) cell lines.

181 presence of either active Ras (Ras(V12)) or EGF.

182 llows the MAPK cascade to transmit paracrine EGF signals into spatially non-uniform ERK activity puls

183 DOTA-Fab-PEG24-EGF or (111)In-DTPA-Fab-PEG24-EGF at the NOAEL, or with unlabeled immunoconjugates or

184 more effectively than (111)In-DTPA-Fab-PEG24-EGF because of a 9.3-fold-higher radiation-absorbed dose

185 (177)Lu-DOTA-Fab-PEG24-EGF bound specifically to HER2 and EGFR on tumor cells.

186 (177)Lu-DOTA-Fab-PEG24-EGF inhibited tumor growth more effectively than (111)In

187 ors were treated with (177)Lu-DOTA-Fab-PEG24-EGF or (111)In-DTPA-Fab-PEG24-EGF at the NOAEL, or with

188 red after exposure to (177)Lu-DOTA-Fab-PEG24-EGF or (111)In-DTPA-Fab-PEG24-EGF or to monospecific (17

189 e growth-inhibited by (177)Lu-DOTA-Fab-PEG24-EGF or (111)In-DTPA-Fab-PEG24-EGF.

190 DOTA-Fab-PEG24-EGF or (111)In-DTPA-Fab-PEG24-EGF or to monospecific (177)Lu- or (111)In-labeled trast

191 um injected amount of (177)Lu-DOTA-Fab-PEG24-EGF that caused no observable adverse effects (NOAEL) wa

192 The binding of (177)Lu-DOTA-Fab-PEG24-EGF to tumor cells (MDA-MB-231, SK-OV-3, MDA-MB-231/H2N,

193 The NOAEL for (177)Lu-DOTA-Fab-PEG24-EGF was 11.1 MBq (10 mug).

194 The tumor uptake of (177)Lu-DOTA-Fab-PEG24-EGF was 2-fold greater than (177)Lu-DOTA-trastuzumab Fab

195 (177)Lu-DOTA-Fab-PEG24-EGF was more cytotoxic than (111)In-DTPA-Fab-PEG24-EGF.

196 ue biodistribution of (177)Lu-DOTA-Fab-PEG24-EGF was studied at 48 h after injection in athymic mice

197 DOTA-Fab-PEG24-EGF or (111)In-DTPA-Fab-PEG24-EGF.

198 s more cytotoxic than (111)In-DTPA-Fab-PEG24-EGF.

199 In response to photoreceptor-EGF, glia produce insulin-like peptides, which induce la

200 ved in the same cells treated with 20-200 pM EGF in vitro.

201 ning endosomes, consistent with preferential EGF-like trafficking through EEA1-containing endosomes.

202 elets release ADAMDEC1, which hydrolyzes pro-EGF to soluble HMW-EGF, that HMW-EGF is active, that pro

203 synthesized as a single 6-kDa domain in pro-EGF, but rather expressed intact pro-EGF precursor on gr

204 in pro-EGF, but rather expressed intact pro-EGF precursor on granular and plasma membranes.

205 Metabolizing pro-EGF Arg(1023) to citrulline with recombinant polypeptide

206 is active, that proteolytic cleavage of pro-EGF first occurs at the C-terminal arginyl residue of th

207 the EGF and the transmembrane domains of pro-EGF.

208 teins showed ADAMDEC1 hydrolyzed surface pro-EGF to HMW-EGF that stimulated HeLa EGF receptor (EGFR)

209 positive and negative feedback loops process EGF signals into ERK pulses of constant amplitude but do

210 ell viability (cytotoxicity), proliferation (EGF + FGF-2) and EMT (TGF-beta1).

211 ated Ras at the plasma membrane and promotes EGF pathways.

212 tains the epithelial growth factor receptor (EGF-R) activation and the expression of ABCC1 multidrug

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

214 g MUC13 and mediated by the first and second EGF-like domains of MUC13.

215 ized in the center of spheroids and secreted EGF, which upregulated alphaMbeta2 integrin on TAMs and

216 related with PI(3,4)P2 levels across several EGF-stimulated prostate and breast cancer lines.

217 of O-glucose or O-fucose stabilizes a single EGF repeat and that addition of both O-glucose and O-fuc

218 we solved the crystal structure of a single EGF repeat covalently modified by a full O-glucose trisa

219 and rate-limiting step in generating soluble EGF bioactivity from activated platelets.

220 Cells treated with soluble EGF demonstrated higher phosphorylated ERK1/2, and cells

221 ld greater persistence compared with soluble EGF.

222 plication of c-Myc siRNAs delivered by SPACE-EGF through the skin can significantly inhibit the growt

223 a new and safe fusion peptide carrier SPACE-EGF to improve the skin and cell penetration function of

224 er cells, the targeting ability of the SPACE-EGF-siRNA complex is increased.

225 In fact, we found platelets did not store EGF, synthesized as a single 6-kDa domain in pro-EGF, bu

226 d phosphorylation of beta-catenin suppressed EGF-mediated epithelial-mesenchymal transition and facil

227 e delayed from Day 21 to Day 42 by switching EGF-containing SHEM to LIF/bFGF-containing MESCM through

228 nsitivity/resistance of inhibitors targeting EGF, MAPK, PI3K, mTOR, and Wnt signaling pathways.

229 or EPGN induce less stable EGFR dimers than EGF-making them partial agonists of EGFR dimerization.

230 ons in planarians, but also demonstrate that EGF signaling likely functions as an essential regulator

231 Our results demonstrate that EGF stimulation can alter intracellular stiffness and po

232 Immunofluorescence revealed that EGF-activated EGFR, MEK1/2 and ERK1/2 co-localize on end

233 with pair-correlation analysis to show that EGF and neuregulin (NRG) can induce different extents of

234 Here, we show that EGF stimulation induces PKCepsilon-dependent phosphoryla

235 These findings suggest that EGF secreted from TAMs plays a critical role in promotin

236 The EGF receptor is a classic receptor tyrosine kinase.

237 The EGF signaling pathway specifies neuronal identities in t

238 F, produced by a single cleavage between the EGF and the transmembrane domains of pro-EGF.

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

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

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

242 hermore, expression of genes involved in the EGF pathway-that is, Ereg, Ltbp4, Matn1, Matn3, and Tpo-

243 Of interest, the EGF signal can be transformed into a differentiating sti

244 urs at the C-terminal arginyl residue of the EGF domain, and that proteolysis is the regulated and ra

245 ures, arising from reduced expression of the EGF family member Epiregulin, which we show is required

246 ed cells with concomitant suppression of the EGF ligand signaling.

247 rs (EGFs) by repressing transcription of the EGF maturation factor rhomboid.

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

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

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

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

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

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

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

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

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

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

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

259 the glycan fills up a surface groove of the EGF with multiple contacts with the protein, providing a

260 Here we show that silencing of the EGF-related factor amphiregulin (AREG) markedly inhibits

261 le genes, and a metagene that represents the EGF pathway was significantly correlated with the presen

262 igand, binds the EGF receptor, reversing the EGF signal to monomerize CAR for its indirect activation

263 d the spindle assembly checkpoint (SAC), the EGF signalling pathway and apoptosis.

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

265 d signaling associated with proximity to the EGF source.

266 he responsiveness of HaCaT and HECV cells to EGF and TGFbeta and resulted in a dysregulation of phosp

267 egulate the responsiveness of these cells to EGF and TGFbeta.

268 Each mutated monomer is fused either to EGF or to an affibody directed against the human EGF rec

269 EGFR phosphorylation under long exposure to EGF.

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

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

272 spond to HGF stimulation, but did respond to EGF.

273 bits Galphas activity in cells responding to EGF.

274 ation with HGF, but had the same response to EGF.

275 ation of the downstream MAPKK in response to EGF.

276 h substrate stiffness, but was responsive to EGF treatment only above a stiffness threshold.

277 ed in mammalian cells to show that these two EGF-CFC homologs have distinct, highly specific ligand b

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

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

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

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

282 well-established and previously undocumented EGF-dependent tyrosine phosphorylation and binding event

283 can distinguish between folded and unfolded EGF repeats raised the possibility that they participate

284 Upon EGF stimulation, GIV modulates Galphai and Galphas seque

285 Upon EGF stimulation, HER3 paralleled previously observed EGF

286 uclear translocation of wild-type SHOC2 upon EGF stimulation, suggesting a more complex function in s

287 The Drosophila egg chamber, where EGF and BMP signaling intersect to specify unique cell t

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

289 estigate this, we used MCF-7 cells, in which EGF-induced transient ERK activation triggers proliferat

290 he authors unravel a mechanism through which EGF stimulation induces MIIP phosphorylation, leading to

291 epidermal growth factor receptor (EGFR) with EGF, the beta2-adrenoceptor with dopamine, or the hepato

292 Crypts incubated with EGF or HGF expanded into self-organizing mini-guts with

293 oximately 25% of sd-rxRNA co-localizing with EGF and <5% with Tf, which is indicative of selective en

294 We made similar observations with EGF, PDGF-AA, and PDGF-BB.

295 nd that TMEFF2, a transmembrane protein with EGF-like and two follistatin-like domains, is selectivel

296 more sustained EGFR signaling than seen with EGF, provoking responses in breast cancer cells associat

297 Adenoma organoids stimulated with EGF or HGF expanded to almost twice the size of nonstimu

298 o IGF-1 alone and to IGF-1 supplemented with EGF (P < 0.001).

299 3D Caco-2 models treated with EGF had increased glucose consumption, production of lac

300 which were not normalized by treatment with EGF.

301 vation of its downstream ERK cascade without EGF stimulation.