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EGFR phosphorylates STAT3. 10 / 99
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"In cervical squamous cell carcinoma, CD109 expression enhanced EGFR-induced phosphorylation of STAT3, resulting in increased tumor aggressiveness and stemness activity [ xref ]."

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"Since EGFR and ERK can directly phosphorylate and activate STAT3, we hypothesized that RPN2 might modulate the activity of STAT3 by EGFR glycosylation."

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"However, we found that TRIM59 overexpression significantly suppressed the interaction of TC45 and STAT3, but increased STAT3 phosphorylation stimulated by EGFRvIII ( xref )."

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"Epidermal growth factor receptor (EGFR)-independent phosphorylation of STAT3 (P-STAT3) has been identified as a mechanism of tumor resistance to agents targeting SFK."

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"In addition, inhibition of EGFR blocked BI-induced Src, Jak2, and STAT3 phosphorylation."

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"EGFR mediated tumor immunoescape : The imbalance between phosphorylated STAT1 and phosphorylated STAT3."

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"These results indicate that EGFRvIII enhances STAT3 transcription and phosphorylation in HNSCC, effects that are resistant to treatment with cetuximab."

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"Meanwhile, Stat3 phosphorylation can be promoted by EGFR ( xref )."

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"In addition, STAT3 functions downstream of the EGFR, and EGFR blocking further inhibits STAT3 phosphorylation."

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"On the cell surface, activated EGFR recruits and phosphorylates STAT3 at Y705, and in turn, phosphorylated STAT3 (p-STAT3) enters the nucleus to activate expression of several cancer-related genes ( xref )."
EGFR phosphorylates STAT3 on Y705. 10 / 10
| 9 1

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"Interestingly, ablation of EGFR and c-RAF expression in NC cells induced increased phosphorylation of STAT3 at the canonical Tyr705 residue (Figure 5C)."

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"2 Phosphorylation of Stat3 at Y705 is often mediated by JAK1, epidermal growth factor receptor, or Src and is required for Stat3 homo- or hetero-dimerization, nuclear translocation, and DNA binding."

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"Phosphorylation of the STAT3 Y705 residue can be induced by cytokines (IL-6, IFN-alpha), growth factors (EGFR, EGFRvIII, HER2 and PDGFR) and non receptor tyrosine kinases (Src and all the JAK family proteins) [XREF_BIBR, XREF_BIBR, XREF_BIBR]."

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"In addition, the presence of EGFR in CHO cells markedly enhanced T. gondii induced early Y705 STAT3 phosphorylation (XREF_SUPPLEMENTARY)."

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"EGFR T790M-cis-L792F mutation upregulated phosphorylation of STAT3 Tyr705 and promoted its specific binding to IL4 promoter, enhancing IL-4 expression and secretion and inducing macrophage M2 polarization."

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"This form of resistance requires dual phosphorylation of STAT3 residues Y705 and S727, mediated by SRC and epidermal growth factor receptor (EGFR), respectively."

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"With regard to signal transducer and activator of transcription 3 (STAT3), cell-surface EGFR and EGFRvIII physically associate with and phosphorylate STAT3 at Y705 and in turn, phosphorylated STAT3 dimerizes and translocates into the cell nucleus to regulate gene expression."

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"With regard to signal transducer and activator of transcription 3 (STAT3), cell-surface EGFR and EGFRvIII physically associate with and phosphorylate STAT3 at Y705 and in turn, phosphorylated STAT3 dimerizes and translocates into the cell nucleus to regulate gene expression."

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"36 A compound binding to the SH2 domain of STAT3 is therefore expected to block the binding of STAT to EGFR and subsequent phosphorylation of Y705 of STAT3."

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"Here, we found that inhibition of EGFR by erlotinib induces STAT3 phosphorylation at Tyr705 in association with increased Bcl2/Bcl-XL at both mRNA and protein levels in various human lung cancer cells."
EGFR phosphorylates STAT3 on tyrosine. 8 / 8
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"STAT3 and STAT1 activation in HER14 cells was demonstrated to depend on EGF receptor kinase activity, rather than JAK2 activity, while in both K721A and CD126 cells (NIH3T3 transfected with kinase-dead EGF receptor, and EGF receptor lacking major autophosphorylation sites, respectively) STAT1 and STAT3 tyrosine phosphorylation requires JAK2 kinase activity."

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"Moreover, STAT3 tyrosine phosphorylation can also be stimulated by EGFR through recruiting to the membrane receptors, except for cytokines, Janus activated kinases (JAK) and Src family kinases XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"STAT3 can also be phosphorylated by multiple upstream molecules, such as receptor tyrosine kinases, vascular endothelial growth factor receptor (VEGFR) and epidermal growth factor receptor (EGFR)."

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"STAT3 is phosphorylated and hence activated by EGF-R and other receptors with intrinsic tyrosine kinase activity as well as by tyrosine kinases associated with transmembrane cytokine receptor family m[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"A77 1726 dose-dependently inhibited total protein tyrosine phosphorylation in uninfected IPEC-DQ (Fig. 4E) and Vero (Fig. 4F) cells.A77 1726 inhibits PEDV replication by inhibiting STAT3 phosphorylation.Yang et al. (2018) reported that PEDV infection of 293T and IPEC-J2 cells rapidly induces STAT3 tyrosine phosphorylation by EGFR tyrosine kinase activation."
| PMC

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"Stimulation of EGFR may induce tyrosine phosphorylation of STAT1, STAT3 and STAT5, initiating complex formation of these STATs with JAK1 and JAK2."

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"A77 1726 dose-dependently inhibited total protein tyrosine phosphorylation in uninfected IPEC-DQ(Fig. 4E)and Vero(Fig. 4F)cells.A77 1726 inhibits PEDV replication by inhibiting STAT3 phosphorylation.Yang et al. (Yang et al., 2018) reported that PEDV infection of 293T and IPEC-J2 cells rapidly induces STAT3 tyrosine phosphorylation by EGFR tyrosine kinase activation."
| PMC

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"However, treatment of the SgK223 overexpressing cells with the selective EGFR tyrosine kinase inhibitor erlotinib did not affect Stat3 activation, despite clear inhibition of EGFR Y1068 phosphorylation, indicating that the enhanced Stat3 tyrosine phosphorylation in SgK223 overexpressing cells was not mediated by the EGFR."
Modified EGFR leads to the phosphorylation of STAT3. 4 / 4
| 4

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"Moreover, ectopic expression of wild type Egfr in cKO-MT cells was sufficient to elevate Stat3 phosphorylation and Aldh1a3 transcript levels (XREF_FIG)."

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"EGFR overexpression induces specifically sustained Stat3 phosphorylation and transcriptional activity."

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"Remarkably, EGFR overexpression, which is frequent in HNSCC cells, not only reduces the level of phosphorylated STAT1 upon the activation of SHP2 but also stimulates the phosphorylation of STAT3, hence promoting the survival, proliferation and dissemination of cancer cells (XREF_FIG)."

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"Taken together, these results demonstrate that overexpression of EGFR mediates specifically sustained Stat3 phosphorylation and transcriptional activity."
Kinase-active EGFR leads to the phosphorylation of STAT3 on Y705. 3 / 3
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"This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth"

"In this paper, we present a comprehensive pathway map of EGFR signaling and other related pathways."

"This is taken from supplemental table 2 from PMID 15951569 Cut-offs were 2.25 for increase and 0.5 for decrease LLID were found by converting from GI assession numbers in DAVID Spreadsheet is saved in the project folder for Cell Signaling Project # bduckworth"
Mutated EGFR leads to the phosphorylation of STAT3 on tyrosine. 2 / 2
| 2

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"These results suggest that activating EGFR mutations may not directly regulate STAT3 tyrosine phosphorylation, since PC9 cells had undetectable STAT3 DNA binding activity."

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"Neither wild-type nor mutant EGFR could increase the levels of tyrosine phosphorylation of STAT3 in these cells (XREF_FIG)."
Modified EGFR leads to the phosphorylation of STAT3 on Y705. 1 / 1
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"To determine if EGFR expression contributed to STAT3 (Tyr705) phosphorylation in vivo, we monitored STAT3 (Tyr705) phosphorylation in the NPcis mouse GEM-PNST compared to NPcis; Wa2/+ mouse GEM-PNSTs."
EGFR leads to the phosphorylation of STAT3 on S727. 1 / 1
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"This form of resistance requires dual phosphorylation of STAT3 residues Y705 and S727, mediated by SRC and epidermal growth factor receptor (EGFR), respectively."
Kinase-active EGFR leads to the phosphorylation of STAT3. 1 / 1
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"Constitutive activation of STAT3 has been shown in human cancers and transformed cell lines. We report that STAT3, but not STAT1 and STAT5, becomes phosphorylated in response to epidermal growth factor (EGF) and achieves maximal induction of collagenase-1 (MMP-1) transcription by interacting with c-JUN"
EGFR leads to the phosphorylation of STAT3 bound to JAK1 and STAT1. 1 / 1
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"Stimulation of EGFR induces Tyr701 phosphorylation of STAT1 and initiates complex formation of STAT1 and STAT3 with JAK1 and JAK2. Thereafter, the STATs translocate to the nucleus within 15 min."