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EGFR phosphorylates STAT3 on tyrosine. 15 / 15
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"The dimerized epidermal growth factor receptor (EGFR) can tyrosine-phosphorylate STAT3, which is elevated in cases of acute lung injury [45] and in cases where STAT1 is lacking [46, 47]."
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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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"JAK and EGFR all phosphorylate Stat3 at the critical tyrosine residue (705) to make it an active form of pSTAT3."
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"A previous study revealed that epidermal growth factor receptor (EGFR) hyperphosphorylated STAT3 through receptor tyrosine kinase activity, inducing its dimerization and translocation to express targe[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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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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"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. (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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"Drug-induced tyrosine phosphorylation of JAK2 and Src attenuated EGFR and STAT3 tyrosine phosphorylation, but EGFR tyrosine kinase inhibitor therapy (gefitinib) suppressed STAT3 phosphorylation in HCT116 colon cancer cells without influencing JAK2 or Src phosphorylation [62]."
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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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"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."
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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 (Fig. 5c), indicating that the enhanced Stat3 tyrosine phosphorylation in SgK223-overexpressing cells was not mediated by the EGFR."
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"Yang et al. (2018) reported that PEDV infection of 293T and IPEC-J2 cells rapidly induces STAT3 tyrosine phosphorylation by EGFR tyrosine kinase activation."
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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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"JAK and EGFR all phosphorylate Stat3 at the critical tyrosine residue (705) to make it an active form of pSTAT3."
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"Hence, these results indicated that monomeric EGFR could phosphorylate STAT3 in the absence of TMEM25 in a tyrosine autophosphorylation-independent manner, giving a good explanation why STAT3 in TMEM25  cells was heavily phosphorylated even without EGF treatment (Fig. 3a and Supplementary Fig. 5a)."
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