ライフサイエンスコーパス: EGF

1 EGF has therapeutic potential to promote human hematopoi

2 EGF induced hydrolysis of nuclear PI(4,5)P(2) by the int

3 EGF is negatively associated with ST muscle phenotype in

4 EGF signaling suppresses the ST phenotype, therefore EGF

5 EGF signaling was (negatively) associated with the ST mu

6 EGF-induced nuclear EGFR localization in DUOX1-deficient

7 and retention of growth factors VEGF (45%), EGF (57%) and TGF-beta1 (42%) on ELISA.

8 ly translocated to the plasma membrane after EGF stimulation.

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

10 1-dependent adaptive CME selectively altered EGF receptor trafficking, enhanced cell migration in vit

11 ith EGFR in vitro and in keratinocytes in an EGF-dependent, integrin-independent manner and that form

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

13 moves at a rate of 85 +/- 33 um/day with an EGF gradient of 16 uM.

14 beta1 upregulating p-p38 but not pERK1/2 and EGF upregulating pERK1/2 but not p-p38.

15 MAPK)) were then examined, and TGF-beta1 and EGF were found to have differential effects on the phosp

16 significant differences between control and EGF-stimulated rates, due to the combination of migratio

17 hages to the tumor and facilitating CSF1 and EGF receptor cross-talk between cancer cells and macroph

18 hase diagram based on local cell density and EGF.

19 for neural induction and the use of FGF2 and EGF for proliferation and it is relatively short as matu

20 a responsiveness to ligands such as GABA and EGF via assembly, stability, and turnover of invadopodia

21 Administration of GH and EGF and their underlying mechanisms were characterized i

22 Circulating and hepatic GH and EGF levels, hepatic damage, and regeneration parameters

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

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

25 activator, and controls cell morphology and EGF-induced membrane protrusion dynamics.

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

27 8 in hepcidin regulation by testosterone and EGF but not inflammation, and suggest a pathogenic role

28 re able to rescue defects in transferrin and EGF internalization caused by loss of endogenous GAPVD1.

29 nes increased endocytosis of transferrin and EGF receptors (TfR and EGFR) concurrent with motility an

30 wth factors (CSF2, IL-6, TNF, HGF, VEGF, and EGF), ATM and p53 signaling pathways.

31 lenges with oncogenic growth factors such as EGF and IL-6.

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

33 sphorylation (pY481) dramatically attenuates EGF-promoted glioma cell proliferation, tumor growth and

34 tion of tumor non-autonomous and -autonomous EGF signaling converts tissue-level feedback into feed-f

35 ead to strong epistatic interactions between EGF and Notch.

36 EGFR signaling, suggesting interplay between EGF- and TGF-beta-signaling pathways during corneal woun

37 was enhanced by collagen and calcium binding EGF domains 1 (CCBE1).

38 actor (EGF) receptor ligand, heparin-binding EGF (HB-EGF), with no defined immuno-pathophysiological

39 the role of the EGFR ligand heparin-binding EGF-like growth factor (HB-EGF) in the beta-cell prolife

40 of one such ligand, soluble heparin-binding EGF-like growth factor (sHB-EGF), also stimulated mouse

41 process is not due to their receptor-binding EGF-like domain, but rather to their distinctive subcell

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

43 tor anastrozole significantly increased both EGF and VEGF (P <0.05).

44 cell surface to facilitate its activation by EGF.

45 vity of FSGS mutants can be downregulated by EGF-mediated phosphorylation, to discern a mechanism by

46 were statistically significantly oxidized by EGF stimulation.

47 pecify cysteines that are redox regulated by EGF stimulation, we performed time-resolved quantificati

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

49 In contrast to normal epithelial cells, EGF stimulation of lung cancer cell lines that lack DUOX

50 in non-apoptotic cells, resulting in chronic EGF signaling.

51 we uncover the essential role of a conserved EGF- and laminin-G-domain-containing protein nlr-1/CASPR

52 gulated by choline availability and controls EGF receptor synthesis and neurogenesis in the cerebral

53 Conversely, EGF receptor signaling in macrophages exacerbated inflam

54 Signal peptide-CUB-EGF domain-containing protein 3 (SCUBE3) is a member of

55 n levels of the EGFR, resulting in defective EGF-dependent signaling and cell migration.

56 Through manipulation of maternally derived EGF and alteration of the earliest gut defenses, we have

57 Thus, maternally derived EGF, and potentially other EGFR ligands, prevents dissem

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

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

60 sly we used gene-editing to label endogenous EGF receptor (EGFR) with GFP and demonstrate that picomo

61 lti-strip model) and migration was excluded, EGF-stimulated cells showed an invasion rate of 21 +/- 3

62 Exogenous EGF reduced GH in steatotic livers, thus activating cell

63 In fact, EGF-induced cellular oxidation of PTP1B was completely d

64 expressing miR-149, epidermal growth factor (EGF) and amphiregulin expression levels were strongly re

65 m dots labeled with epidermal growth factor (EGF) and demonstrate the necessity of near-infrared emis

66 important ligands, epidermal growth factor (EGF) and hepatocyte growth factor (HGF), and across wide

67 er stimulation with epidermal growth factor (EGF) and that bicarbonate levels directly correlate with

68 Moreover, epidermal growth factor (EGF) failed to suppress hepcidin in Smad15;Alb-Cre(+) he

69 s the source of the epidermal growth factor (EGF) family member NEUREGULIN1 (NRG1).

70 H through exogenous epidermal growth factor (EGF) in steatotic and nonsteatotic grafts.

71 In PC12 cells, epidermal growth factor (EGF) induces transient ERK activation that leads to cell

72 Epidermal growth factor (EGF) maintains intestinal stem cell (ISC) proliferation

73 d concentrations of epidermal growth factor (EGF) of maternal origin within the intestinal tract of m

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

75 c administration of epidermal growth factor (EGF) promoted HSC DNA repair and rapid hematologic recov

76 back control of the epidermal growth factor (EGF) protease Rhomboid (Rho).

77 Activation of the epidermal growth factor (EGF) receptor (EGFR) at the cell surface initiates signa

78 T cells express the epidermal growth factor (EGF) receptor ligand, heparin-binding EGF (HB-EGF), with

79 cargos, such as the epidermal growth factor (EGF) receptor, along the endocytic pathway.

80 stablished that the epidermal growth factor (EGF) receptor, receptor tyrosine-protein kinase erbB-2 (

81 yr kinase domain of epidermal growth factor (EGF) receptor.

82 Additionally, epithelial growth factor (EGF) signaling suppresses 15-PGDH expression while simul

83 that trafficking of epidermal growth factor (EGF) to late endosomes and degradation of its receptor w

84 upon stimulation by epidermal growth factor (EGF) to reduce the binding to actin cytoskeleton.

85 We have found that epidermal growth factor (EGF) triggered an enrichment of ORAI1 at the leading edg

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

87 In contrast, epidermal growth factor (EGF) was significantly downregulated in a subgroup of DO

88 Upon addition of epidermal growth factor (EGF), both ESCRT-I and Vps4 are retained at endosomes fo

89 in growth factor (epithelial growth factor (EGF), hepatocyte growth factor (HGF)) and the activation

90 by IFN-gamma (MIG), epidermal growth factor (EGF), hepatocyte growth factor (HGF), vascular endotheli

91 Luciferase (GLuc), epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha) and e

92 inuing 3D growth in epidermal growth factor (EGF)-containing medium for 4 weeks results in antral hGO

93 r 5 (ETV5) mediates epidermal growth factor (EGF)-induced hTERT expression in MCF10A cells.

94 ole of PLCdelta4 in epidermal growth factor (EGF)-induced nuclear Ca(2+) signaling and downstream eve

95 chanism, we utilize epidermal growth factor (EGF)-inducible immediate early genes (IEGs).

96 separate the first epidermal growth factor (EGF)-like domain from the remainder of the protein.

97 PvMSP1P), which has epidermal growth factor (EGF)-like domains, was identified as a novel erythrocyte

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

99 tigated the role of epidermal growth factor (EGF)-like repeats and discoidin-like domains 3 (EDIL3) a

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

101 changes, including epidermal growth factor (EGF).

102 density in reduced epidermal growth factor (EGF).

103 g overexpression of epidermal growth factor (EGF).

104 R isoforms bind the epidermal growth factor (EGF).

105 r-beta [TGF-beta1], epidermal growth factor [EGF], platelet-derived growth factor AB [PDGF-AB], and a

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

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

108 as was the incidence of early graft failure (EGF).

109 ikely being involved in TGF-beta/BMP and FGF/EGF signaling pathways.

110 s activated proteolytic release of the first EGF-like repeat, suggesting that the elimination of mult

111 growth factor receptor (EGFR) is crucial for EGF-induced receptor activation.

112 ], and the duration of CPR discriminated for EGF [AUC of 0.86 (95% CI, 0.74-0.98)], with a sensitivit

113 at formation of this complex is required for EGF-dependent migration.

114 nation and activation, which is required for EGF-induced Akt mitochondrial localization.

115 In vitro, TMEM16A is required for EGF-induced store-operated calcium entry essential for p

116 >15 min increased over 5 times the risk for EGF [HR 5.80 (95% CI, 1.82-18.56); P = 0.003], and these

117 CAT increased the risk for EGF [OR 1.09 (95% CI, 1.01-1.17)], and the duration of C

118 These data agree with the role for EGF replacement therapy in EGF-deficient individuals wit

119 04 promoted EGFR endocytosis distinctly from EGF: it was asynchronous, not accompanied by canonical s

120 ase in coding region mutations in HSPCs from EGF-treated mice, but increased intergenic copy number v

121 Further, EGF treatment drove the recovery of human HSCs capable o

122 Further, EGF-stimulated membrane recruitment of tSH2-WT differed

123 Furthermore, EGF induced three distinct spatiotemporal patterns of cy

124 Furthermore, EGF-induced plasma membrane ERK activity involves Rap1,

125 -like domains 3 (EDIL3) and milk fat globule-EGF factor 8 (MFGE8), two glycoproteins that are consist

126 cid cleavage product of the milk fat globule-EGF factor 8 protein, is one of the most common forms of

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

128 HB-EGF coimmunoprecipitates with the transcriptional repres

129 GF) receptor ligand, heparin-binding EGF (HB-EGF), with no defined immuno-pathophysiological function

130 idermal growth factor-like growth factor (HB-EGF) as the signal that maintains HSC quiescence and sho

131 d heparin-binding EGF-like growth factor (HB-EGF) in the beta-cell proliferative response to glucose,

132 idermal growth factor like growth factor (HB-EGF), a crucial regulator of heart valve development in

133 idermal growth factor-like growth factor (HB-EGF), a potent epithelial proliferation and migration st

134 Our findings identify a novel glucose/HB-EGF/EGFR axis implicated in beta-cell compensation to in

135 c family kinases, known to be involved in HB-EGF processing, abrogated glucose-induced beta-cell prol

136 n immunoregulatory function for intrinsic HB-EGF expressed by CD4 T cells in T(H)2 inflammation and a

137 f of concept that local administration of HB-EGF has the potential to be developed as a topical treat

138 Furthermore, knockdown of HB-EGF in rat islets blocks beta-cell proliferation in resp

139 e, we wished to elucidate the function of HB-EGF synthesized by CD4 T cells in the context of allergi

140 BL/6 J mice, we evaluated the efficacy of HB-EGF treatment (5 ul of 10 ug/ml) solution.

141 In rat islets, inhibition of EGFR or HB-EGF blocks the proliferative response not only to HB-EGF

142 In this study, we show how knocking out HB-EGF expression in CD4 T cells in vivo attenuates IL-5 sy

143 Knocking out HB-EGF in CD4 T cells resulted in increased Bcl-6 binding t

144 ow that immature LSECs are unable to shed HB-EGF from the cytosolic membrane.

145 The results show that HB-EGF delivered post radiation, significantly increased th

146 Mechanistically, we demonstrate that HB-EGF mRNA levels are increased in beta-cells in response

147 ChREBP binding sites in proximity to the HB-EGF gene.

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

149 ks the proliferative response not only to HB-EGF but also to glucose.

150 osure of isolated rat and human islets to HB-EGF stimulates beta-cell proliferation.

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

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

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

154 However, EGF increased GH in nonsteatotic grafts, which exacerbat

155 tyrosine-protein kinase erbB-2 (ERBB2)/human EGF receptor 2 (HER2), and, to a lesser extent, ERBB4/HE

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

157 Importantly, EGF and oncogenic KRAS induce OTUB2 poly-SUMOylation and

158 In EGF-activated cells, NRas clusters became more diffused

159 A expression resulted in similar deficits in EGF degradation, accumulation in a RAB4 compartment, and

160 GDH1-mediated glutaminolysis was involved in EGF-promoted cell proliferation.

161 ole of Fyn-dependent 6PGD phosphorylation in EGF-promoted tumor growth and radiation resistance.

162 with the role for EGF replacement therapy in EGF-deficient individuals with AD as well as DOCK8 defic

163 rone supplementation significantly increased EGF levels in tissue samples, whereas when combined with

164 pancreas transplantation without increasing EGF risk, and in those with longer CAT it may be prudent

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

166 es, including DUSP1, 5, and 6, and inhibited EGF/MAPK signaling.

167 The effect was reversible by inhibiting EGF or activating TGFbeta signaling.

168 rk highlights the complexities of intestinal EGF/ERBB signaling and delineates key niche cells and si

169 , we identified neuregulin 1 (NRG1) as a key EGF family ligand that drives tissue repair following in

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

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

172 nked to AML-relevant signaling pathways like EGF/EGFR and Wnt/Hedgehog/Notch.

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

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

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

176 l homeostasis, suggesting roles for multiple EGF family ligands in ISC function.

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

178 cle phenotype in mice and humans, and muscle EGF transcript levels were raised in COPD.

179 NRG1, but not EGF, is upregulated upon damage and is expressed in mese

180 g intestine enteroid cultures, NRG1, but not EGF, permitted increased cellular diversity via differen

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

182 Sustained activation of EGF receptor (EGFR) in proximal tubule cells is a hallma

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

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

185 The benefits of EGF for steatotic grafts were associated with increased

186 ndary tier of signaling networks composed of EGF and TGFbeta.

187 < 0.001) and higher serum concentrations of EGF (epithelial growth factor), GM-CSF, IL-10, CCL2/MCP-

188 es or on endocytosis-mediated degradation of EGF receptor.

189 ms through transcriptional downregulation of EGF, which resulted in decreased EGFR phosphorylation.

190 Here we examine the effect of EGF on transforming growth factor-beta receptor II (TGF-

191 Expression of EGF family members increased when Tgfb1 was repressed in

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

193 measure cell movement under the influence of EGF (chemoattractant) gradients.

194 Endocan is a novel and critical regulator of EGF/EGFR signaling and serves as an alternative target o

195 ow that SMURF2 extends membrane retention of EGF-bound EGFR, whereas SMURF2 knockdown increases recep

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

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

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

199 er, protein kinase C, a downstream target of EGF, was active in the nucleus of stimulated cells.

200 Organoid growth is dependent on EGF and Wnt activators.

201 In contrast, persistent EGF-dependent translocation of RAF1-mVenus to the plasma

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

203 FR endocytosis stimulated with physiological EGF concentrations.

204 EDIL3 and MFGE8 proteins possess EGF-like and coagulation factor 5/8 (F5/8C) domains, and

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

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

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

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

209 g cancer cell lines that lack DUOX1 promotes EGF-induced EGFR internalization and nuclear localizatio

210 YAP5SA, but not inactive Mt-YAP6SA, promotes EGF-independent proliferation and tumorigenesis in BRCA1

211 nfirmed by competition experiment using pure EGF protein.

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

213 Interestingly, administration of recombinant EGF rescued mice from IDO1 inhibition-driven aggravated

214 were strongly reduced, resulting in reduced EGF receptor activation in the cancer cells.

215 cells display diminished motility in reduced EGF, which permits irreversible adhesion upon cell-cell

216 isintegrin and metalloprotease 17) regulates EGF-receptor and TNFalpha signaling, thereby not only pr

217 Together, these findings reveal EGF as a potential therapeutic intervention for infectio

218 Because Rho, EGF receptor (EGFR), and E-cad are associated with color

219 o in apoptotic cells enables them to secrete EGFs, which stimulate nearby stem cells to undergo repla

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

221 sHB-EGF also increased muscle EGFR protein expression and ac

222 sHB-EGF expression was concentrated at the neuromuscular jun

223 sHB-EGF increased TFAP4 binding to this site in muscle cells

224 heparin-binding EGF-like growth factor (sHB-EGF), also stimulated mouse muscle Galgt2 gene expressio

225 TFAP4-binding site that was required for sHB-EGF activation.

226 These data demonstrate that sHB-EGF is an endogenous regulator of muscle Galgt2 gene exp

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

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

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

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

231 FR) in tissues, we generated an sfGFP-tagged EGF receptor (EGFR-sfGFP) in Drosophila The homozygous f

232 These studies demonstrate that EGF promotes HSC DNA repair and hematopoietic regenerati

233 These results provide evidence that EGF-induced nuclear signaling is mediated by nuclear PLC

234 tatus of EGFR, as evidenced by the fact that EGF fails to induce EGFR phosphorylation in GP78-deficie

235 We found that EGF-induced Ca(2+) signals are inhibited when translocat

236 Taken together, these data indicate that EGF stimulates TGF-betaRII through ERK1/2 and EGFR signa

237 Using these sensors, we showed that EGF induces sustained ERK activity near the plasma membr

238 The EGF receptor (EGFR) is widely expressed in the kidney in

239 The EGF signaling pathway specifies neuronal identities in t

240 how here that sSORLA binds and activates the EGF receptor to induce downstream signaling through the

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

242 throid lineage, which reveals a role for the EGF receptor family member, ErbB4, as an important media

243 Recent studies have identified the EGF receptor (EGFR) ligand amphiregulin (AREG) as an imp

244 EHD1 or RUSC2 depletion impaired the EGF-induced cell proliferation, demonstrating that the n

245 movement in the presence and absence of the EGF chemoattractant.

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

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

248 trated that it dampens the activation of the EGF pathway.

249 versus sustained signaling downstream of the EGF receptor (EGFR) and NGF receptor (TrkA).

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

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

252 ollagen production through inhibition of the EGF receptor (EGFR) that phosphorylates cytoplasmic and

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

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

255 erformed time-resolved quantification of the EGF-dependent oxidation of 4200 cysteine sites in A431 c

256 ling via direct binding and enhancing of the EGF-EGFR interaction and supported the growth of tumors

257 ulation by cleaving the alpha subunit of the EGF-like module-containing mucin-like hormone receptor-l

258 EGFL6, a member of the EGF-like superfamily, plays an important role during emb

259 glucosylated peptides were identified on the EGF domain from nine proteins.

260 that PFKFB3 inhibition markedly reduces the EGF-mediated increase in glycolysis.

261 lacking protease activity (but retaining the EGF-like domain) was as effective as wild-type tPA in re

262 Here, we report that the EGF-like domain I within the extracellular domain of EpC

263 n promoting neurite regeneration through the EGF receptor/ERK/Fos pathway, thereby demonstrating a po

264 leased by proteolytic cleavage, bound to the EGF receptor (EGFR) on cancer cells inducing EGFR phosph

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

266 d signaling associated with proximity to the EGF source.

267 Using the EGF-EGFR signaling axis as a model in MDA-MB-231T cells,

268 This EGF-like domain (PvMSP1P-19) elicited high level of acqu

269 icrobiome-derived, metabolite levels through EGF receptors and downstream signaling to induce their s

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

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

272 response of CHORDC1-deficient A431 cells to EGF stimulation is attenuated, the EGFR accumulates in t

273 he K225E after extended exposure of cells to EGF, with a decrease in ACTN4 aggregates in fibroblasts.

274 cells harboring either WT or mutated EGFR to EGF rapidly increases PFKFB3 phosphorylation, expression

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

276 quency of ERK pulses, and the sensitivity to EGF stimuli.

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

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

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

280 FBXW2 binds to beta-catenin upon EGF-AKT1-mediated phosphorylation on Ser(552), and promo

281 lustering of NRas and BRAF was observed upon EGF activation.

282 nd impact on phosphoproteome remodeling upon EGF stimulation.

283 rat liver transplant from BD donors, whereas EGF (throughout GH inhibition) protects only in steatoti

284 source of WNT and RSPONDIN ligands, whereas EGF is expressed far from crypts in the villus epitheliu

285 trates served as two distinct modes by which EGF specified the cryptic cysteine residues that became

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

287 C cell proliferation, which is enhanced with EGF receptor (EGFR) inhibition.

288 egative control, contrasting expression with EGF stimulation against expression without EGF stimulati

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

290 rkers were quantified in C2C12 myotubes with EGF-neutralizing antibody, EGFR inhibitor or an EGFR-sil

291 share a common structural organization with EGF-like and SEA domains.

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

293 In DLD-1 cells stimulated with EGF, SHOC2 function is essential for a rapid transient p

294 Primary HCE were treated with EGF +/- U0126 (MEK inhibitor) and assayed for TGF-betaRI

295 When pHCE were treated with EGF for 6 hours, the cells produced enhanced levels of T

296 3D Caco-2 models treated with EGF had increased glucose consumption, production of lac

297 Here, we report that treatment with EGF and a GSK3 inhibitor thinned the circumferential F-a

298 vation of its downstream ERK cascade without EGF stimulation.

299 h EGF stimulation against expression without EGF stimulation.

300 cells provide multiple secreted (e.g., Wnt, EGF) as well as surface-bound (Notch ligand) niche signa