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1 tive interdomain pocket of the extracellular 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 es or on endocytosis-mediated degradation of EGF receptor.
6 ory role of CD82 in endocytic trafficking of EGF receptor.
7 increased EGF-induced phosphorylation of the EGF receptor.
8 ce and depends on the kinase activity of the EGF receptor.
9 phorylated and associated with the activated EGF receptor.
10 B domain of Shc (SHC adaptor protein) to the EGF receptor.
11 rlotinib, a clinically used inhibitor of the EGF receptor.
12 ion of the receptor tyrosine kinases MET and EGF receptor.
13 h direct binding and activation of the renal EGF receptor.
14 he binding of Grb2 and Shc to the single-Tyr EGF receptors.
15 d signaling via the epidermal growth factor (EGF) receptor.
16 yr kinase domain of epidermal growth factor (EGF) receptor.
17 tyrosine-protein kinase erbB-2 (ERBB2)/human EGF receptor 2 (HER2), and, to a lesser extent, ERBB4/HE
19 l Growth Factor Receptors (EGFR) or to human EGF receptors 2 (HER2), which are overexpressed in sever
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
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
27 imer formation, suggesting that its path for EGF receptor activation involves binding to both monomer
30 tered downstream of epidermal growth factor (EGF) receptor activation, following the phosphorylation
31 ferences in network utilization by different EGF receptor agonists and highlight the need to characte
34 require the tyrosine kinase activity of the EGF receptor and are mediated by complexes containing ac
35 l sulfate and p-cresol sulfate activated the EGF receptor and downstream signaling by enhancing recep
36 racterized the interaction of ErbB3 with the EGF receptor and ErbB2 and assessed the effects of Food
40 samples from patients with CD was reduced by EGF receptor and IL15 blocking antibodies only when used
41 ol sulfate significantly activated the renal EGF receptor and increased the tubulointerstitial expres
42 re an active block to signal transduction by EGF receptor and LIN-12/Notch and have a different mecha
43 epidermal growth factor (EGF) share the same EGF receptor and previously indistinguishable intracellu
44 eptor tyrosine kinase acts downstream of the EGF receptor and Src tyrosine kinases to promote invadop
46 icrobiome-derived, metabolite levels through EGF receptors and downstream signaling to induce their s
47 isintegrin and metalloprotease 17) regulates EGF-receptor and TNFalpha signaling, thereby not only pr
48 a leads to aberrant activation of TAK1, JNK, EGF receptor, and ERK in distinct microanatomical areas
50 ronectin interactions on the efficacy of the EGF receptor antibody cetuximab, which is used widely fo
52 mice administered cetuximab, an inhibitor of EGF receptor binding, and (b) immunological data showing
53 se to certain growth factor receptors (i.e., EGF-receptor but not insulin receptor) and pathogen reco
55 uently, we analyzed changes in expression of EGF receptors, cell aspect ratio, and protrusive activit
56 hages to the tumor and facilitating CSF1 and EGF receptor cross-talk between cancer cells and macroph
61 The role of endocytosis in the control of EGF receptor (EGFR) activation and cell signaling was ex
63 ity was accompanied by reduced expression of EGF receptor (EGFR) and an increased degradation rate of
64 geting of prominent cancer antigens, such as EGF receptor (EGFR) and c-MET, by bsAbs has raised incre
65 ion of its chloride-channel activity reduced EGF receptor (EGFR) and calmodulin-dependent protein kin
67 phosphorylation of specific tyrosines in the EGF receptor (EGFR) and in inefficient activation of the
72 n that MUC1-C, in turn, forms complexes with EGF receptor (EGFR) and promotes EGFR-mediated activatio
73 racellular domain of NRP1 interacts with the EGF receptor (EGFR) and promotes its signaling cascade e
75 ed by temporal compensatory increases in the EGF receptor (EGFR) and the hepatocyte growth factor rec
76 odimeric IgG derived from anti-HER2 and anti-EGF receptor (EGFR) antibody was shown to induce a highe
77 sine kinase inhibitors (TKI) that target the EGF receptor (EGFR) are effective in most non-small cell
80 nctions as a tumor suppressor that restricts EGF receptor (EGFR) cell surface occupancy as well as Ak
81 udy a mechanism by which dimerization of the EGF receptor (EGFR) cytoplasmic domain is transmitted to
83 Stress exposure triggers ligand-independent EGF receptor (EGFR) endocytosis, but its post-endocytic
84 sponse to LPS is impaired by down regulating EGF receptor (EGFR) expression or by using the EGFR inhi
88 en by signature genetic alterations, such as EGF receptor (EGFR) gene amplification and mutation, pla
90 Tyrosine kinase inhibitors (TKIs) of the EGF receptor (EGFR) have provided a significant improvem
92 e ligands on subunit-subunit interactions in EGF receptor (EGFR) homodimers and EGFR/ErbB2 heterodime
95 dying enterocyte triggers activation of the EGF receptor (Egfr) in stem cells within a discrete radi
98 We therefore examined the effects of the EGF receptor (EGFR) inhibitor erlotinib on liver fibroge
100 ening assay prompted us to determine whether EGF receptor (EGFR) inhibitors stimulate AQP2 traffickin
102 role in the trafficking of the ligand-bound EGF receptor (EGFR) internalized through receptor-mediat
105 dermal growth factor (EGF) activation of the EGF receptor (EGFR) is an important mediator of cell mig
109 ously established that overexpression of the EGF receptor (EGFR) is sufficient to induce tumor format
112 lung cancer with activating mutations in the EGF receptor (EGFR) kinase, who are treated long-term wi
113 n-induced type 1 diabetes, podocyte-specific EGF receptor (EGFR) knockout mice (EGFR(podKO)) and thei
116 elevance of iRhom2 in regulating shedding of EGF receptor (EGFR) ligands is established by a lack of
117 leased by proteolytic cleavage, bound to the EGF receptor (EGFR) on cancer cells inducing EGFR phosph
118 or (EGF), leading to decreased activation of EGF receptor (EGFR) on target cells and, eventually, dam
122 ect targets of miR-148a were identified, the EGF receptor (EGFR) regulator MIG6 and the apoptosis reg
123 face pro-EGF to HMW-EGF that stimulated HeLa EGF receptor (EGFR) reporter cells and EGFR-dependent tu
124 tumors harboring activating mutations in the EGF receptor (EGFR) show good initial treatment response
125 the role of the Tid1 isoforms in regulating EGF receptor (EGFR) signaling and lung cancer progressio
126 disintegrin and metalloprotease 17) controls EGF receptor (EGFR) signaling by liberating EGFR ligands
127 ay dependence or (ii) constitutive autocrine EGF receptor (EGFR) signaling driven by c-Jun-mediated E
128 evels of functional proteins associated with EGF receptor (EGFR) signaling in pairs of U87EGFR varian
133 ollagen production through inhibition of the EGF receptor (EGFR) that phosphorylates cytoplasmic and
134 ype 1 matrix metalloproteinase (MT1-MMP) and EGF receptor (EGFR) to the cell surface during invadopod
136 eta1-adrenergic receptor stimulation-induced EGF receptor (EGFR) transactivation in addition to Gbeta
140 or-activated receptor, because inhibition of EGF receptor (EGFR) with cetuximab or EGF-depleted amnio
141 sly we used gene-editing to label endogenous EGF receptor (EGFR) with GFP and demonstrate that picomo
142 diated enhanced HCV entry and endocytosis of EGF receptor (EGFR), an HCV entry cofactor and erlotinib
144 teracts with a variety of kinases (PKC, FES, EGF receptor (EGFR), and JAK3) that are activated by it,
145 SCs from wild-type mice expressed functional EGF receptor (EGFR), and systemic administration of EGF
147 imulates TGFbeta signaling and activates the EGF receptor (EGFR), but the relative contribution of th
148 le receptor-tyrosine kinases (RTKs), such as EGF receptor (EGFR), ErbB-2, FGF receptor (FGFR), and ma
149 r (EGF)-like ligand that signals through the EGF receptor (EGFR), in both osteoblasts and osteocytes.
150 like growth factor (HB-EGF), a ligand of the EGF receptor (EGFR), in nutrient-induced beta-cell proli
151 se tumors harbor activating mutations in the EGF receptor (EGFR), increased responses to platinum-bas
152 ke growth factor (HBEGF) is a ligand for the EGF receptor (EGFR), one of the most commonly amplified
154 (HGF)/MET and epidermal growth factor (EGF)/EGF receptor (EGFR), two key signal transduction systems
155 ein (Vn) is a neuregulin-like ligand for the EGF receptor (Egfr), which is necessary for global devel
156 first six amino acids of this segment of the EGF receptor (EGFR), which lies in close association wit
158 (UTMD) could be used to enhance delivery of EGF receptor (EGFR)-directed siRNA to murine squamous ce
161 and neck (HNSCC) overexpress ERBB1/EGFR, but EGF receptor (EGFR)-targeted therapies have yielded disa
162 ion as a mechanism of acquired resistance to EGF receptor (EGFR)-targeted therapies in non-small cell
164 e use luciferase fragment complementation in EGF receptor (EGFR)/ErbB2 heterodimers to probe the mech
165 the autocrine or paracrine activation of the EGF receptor (EGFR)/mitogen-activated protein/extracellu
166 ment by crawling depends on signaling by the EGF receptor (EGFR); however, this was not required for
167 FR) in tissues, we generated an sfGFP-tagged EGF receptor (EGFR-sfGFP) in Drosophila The homozygous f
168 CERT determines the signaling output of the EGF receptor (EGFR/ErbB1), which is upregulated in appro
169 ErbB family members, such as ErbB2 (HER2) or EGF receptor (EGFR; HER1), enhancing phosphorylation of
171 trigger the release of ligands that activate EGF receptors (EGFR) on the granulosa, thereby initiatin
172 degradation of the epidermal growth factor (EGF) receptor (EGFR) after its activation and internaliz
173 Activation of the epidermal growth factor (EGF) receptor (EGFR) at the cell surface initiates signa
175 ain shedding of the epidermal growth factor (EGF) receptor (EGFR) ligand heparin-binding EGF-like gro
176 aling proteins with epidermal growth factor (EGF) receptors (EGFR) using biotinylated EGF bound to st
177 s the expression of epidermal growth factor (EGF) receptors (EGFR, ERBB3) and production of EGF-like
179 ciated pool colocalizes with transferrin and EGF receptors (EGFRs) and early endosome antigen 1, but
181 ifference in the rates of degradation of the EGF receptor (ErbB1) and ErbB2 upon treatment of cells w
182 ur study also shows that all pairings of the EGF receptor, ErbB2, and ErbB3 form ligand-independent d
183 n of several tumor-enhancing RTKs, including EGF receptor, ErbB2, hepatocyte growth factor receptor (
184 GPER-mediated signaling, which involved the EGF receptor/ERK/c-Fos/AP1 transduction pathway, as asce
185 n promoting neurite regeneration through the EGF receptor/ERK/Fos pathway, thereby demonstrating a po
187 eceptor, they bound poorly to the single-Tyr EGF receptors, even those that bound full-length Grb2 an
188 rotein (GFP)-tagged epidermal growth factor (EGF) receptor expressed in Jurkat cells with immobilized
189 throid lineage, which reveals a role for the EGF receptor family member, ErbB4, as an important media
191 planation for the apparent preference of the EGF receptor for dimerizing with ErbB2 and suggest that
193 Accordingly, reduction in the levels of the EGF receptor gene contributes to the activation of Esrrb
197 R2 heterodimerizes with other members of the EGF receptor/HER/ErbB family, and the HER2-HER3 dimer fo
198 is study provides valuable insights into the EGF receptor/HER/ErbB kinase structure and interactions,
200 increased plasma membrane expression of the EGF receptor in resting cells and increased EGF-induced
205 detect upregulated epidermal growth factor (EGF) receptor in orthotopic pancreatic xenografts using
206 tivation by mutant TRPC6, a cell-autonomous, EGF receptor-independent mechanism and a non-cell-autono
207 e signaling capabilities of these single-Tyr EGF receptors indicated that they can activate a range o
208 s lysosomal targeting and degradation of the EGF receptor, indicating that it targets host-membrane t
211 genous AMF overcame the inhibitory effect of EGF receptor inhibitor gefitinib on invasive motility by
214 n of downstream effector pathways shows that EGF receptor inhibits the Hippo pathway through activati
218 mainly known as a negative regulator of the EGF receptor, is an important mediator of progesterone s
219 ated in the spatiotemporal regulation of the EGF receptor, is required for TRAIL-induced cell death i
220 tors, including the epidermal growth factor (EGF) receptor, is key to various cellular processes, suc
221 surface precursor of an alternately spliced EGF receptor isoform and that sEGFR binds to EGF with hi
223 appaB activated by oncogenes such as Ras and EGF receptor leads to cell-autonomous effects, abrogatin
226 m knockdown results in overexpression of the EGF receptor ligand vein (vn), which further activates E
228 T cells express the epidermal growth factor (EGF) receptor ligand, heparin-binding EGF (HB-EGF), with
229 erting enzyme, is the major sheddase for the EGF receptor ligands and is considered to be one of the
230 different growth factors suggests that these EGF receptor ligands fall into two major groups as follo
231 ferences in biological response to different EGF receptor ligands may result from partial agonism for
232 lar peptides (C-type natriuretic peptide and EGF receptor ligands) maintain the low level of cGMP in
236 y and which tyrosines are required to enable EGF receptor-mediated signaling, we generated a series o
237 N-glycans restricts epidermal growth factor (EGF) receptor mobility in the plasma membrane and acts s
238 LaS3 cell lines, as well as H1975 activating-EGF receptor mutant lung cancer cell resulted in dephosp
240 ta subunits was blocked by inhibition of the EGF receptor or STAT3 but not by the PI3K/AKT or MEK/ERK
241 nes were linked to the Wnt, Hippo, TGF-beta, EGF receptor, or PI3K pathways, all involved in colorect
244 nt advances in our understanding of the AREG-EGF receptor pathway and its involvement in infection an
245 is revealed that the presence of a synthetic EGF receptor peptide significantly decreased the spectro
246 t also elicited prosurvival signaling via an EGF receptor/phosphoinositide 3-kinase (PI3K) pathway.
247 ation tissue area, vascularity, and IGF1 and EGF receptor phosphorylation are increased in GM3S SNA-t
248 ransferrin from endosomes, or degradation of EGF receptor proceeds unperturbed in cells with impaired
249 ith deep-seated gliomas that overexpress the EGF receptor produced an estimate of available receptor
250 stablished that the epidermal growth factor (EGF) receptor, receptor tyrosine-protein kinase erbB-2 (
251 rbital, which is not a CAR ligand, binds the EGF receptor, reversing the EGF signal to monomerize CAR
252 s "checkpoint." Dysregulated CME also alters EGF receptor signaling and leads to constitutive activat
254 breast cancer, emphasizing the importance of EGF receptor signaling in breast tumor pathogenesis and
256 proliferative activities along with enhanced EGF receptor signaling in the articular cartilage and in
258 beta cells but also release EGF to activate EGF receptor signaling that inhibits TGFbeta1-activated
259 ed for SREBP-1 activation by angiotensin II, EGF receptor signaling was necessary for activation of t
261 reased expression of gene pathways mediating EGF receptor signaling, circadian exercise, striated mus
268 to drugs that block epidermal growth factor (EGF) receptor signaling could be caused by aberrant acti
269 n-regulated nuclear epidermal growth factor (EGF) receptor signaling in the CySC lineage is essential
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
273 epithelial invasion by derepressing upstream EGF receptor, SRC tyrosine kinase, and phosphoinositide
274 Our findings reveal a novel link between EGF receptor stimulation, ILK-containing complexes, and
275 signaling via both the TGFbeta-receptor and EGF receptor suggesting that PAR2 utilizes transactivati
276 e F-BAR-domain protein PACSIN2 in regulating EGF receptor surface levels and EGF-induced downstream s
277 gulated by choline availability and controls EGF receptor synthesis and neurogenesis in the cerebral
279 nes increased endocytosis of transferrin and EGF receptors (TfR and EGFR) concurrent with motility an
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 how here that sSORLA binds and activates the EGF receptor to induce downstream signaling through the
286 r a MAPK signaling cascade downstream of the EGF receptor to investigate how interlinked positive and
287 gether, our studies reveal a crucial link of EGF receptor to NF-kappaB activation and tumor progressi
288 localization of the epidermal growth factor (EGF) receptor to the plasma membrane, prolonging EGF sig
289 1-dependent adaptive CME selectively altered EGF receptor trafficking, enhanced cell migration in vit
290 ents autocrine ligand shedding and resultant EGF receptor transactivation, it also leads to an accumu
291 internalized EGF as well as the (activated) EGF receptor translocated to PACSIN2-positive endosomes.
292 s to cell surface antigens including MET and EGF receptor, we have experimentally validated our model
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
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