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EGF phosphorylates STAT3. 10 / 162
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"An im-portant finding in our study was the demonstration of increased EGF stimulated phosphorylation of multiple SFKs and STAT3 in cells lacking Sh3gl2, both of which have been implicated in urothelia[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Both HIF-1α and EGF-induced phosphorylation of STAT3 could significantly promote the proliferation and metastasis of SW480, and enhance tumorigenesis."

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"Mutation of this residue to phenylalanine, which can not be phosphorylated (Y845F), did not affect EGF stimulated phosphorylation of phospholipase C, MAPK, or STAT3, but completely suppressed phosphorylation of STAT5b at its activating tyrosine, Y699 [XREF_BIBR]."

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"Furthermore, we found that silibinin suppressed the EGF-induced phosphorylation of STAT3 but not Erk and Akt."

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"Correspondingly, the expression of the pro-survival form of Fas enhanced the EGF-induced phosphorylation of STAT3, which is important for the cancer-promoting activities, such as migration of colorectal cancer cells (Figs  xref and xref )."

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"Here we showed that AKT was highly phosphorylated within 5 min after EGF stimulation, and treatment with API2, a pharmacological inhibitor of AKT, reduced EGF-induced STAT3 phosphorylation and CCR1 mRNA expression."

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"As shown in XREF_FIG, EGF triggered an increase in the phosphorylation of STAT3, AKT, ERK1/2, and p38 as early as 15min and sustained for 4h (except p-ERK1/2); the phosphorylation started declining 8h after the treatment."

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"After 24 and 48 hrs of vemurafenib treatment, however, EGF activates MEK, ERK, AKT, and STAT3 phosphorylation."

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"Consistent with the calcium chelation experiments, a significant reduction in EGF-induced STAT3 phosphorylation was a consequence of TRPM7 silencing in MDA-MB-468 breast cancer cells ( xref )."

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"Therefore, for the first time, we suggest that the JAK3 inhibitor, WHI-P131, inhibits EGF-induced STAT-3 phosphorylation as well as ERK phosphorylation."
EGF phosphorylates STAT3 on tyrosine. 10 / 11
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"Pretreatment with Wit for as little as 2-10min inhibited EGF stimulated STAT3 tyrosine phosphorylation partially, and complete inhibition occurred within 15-30min."

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"We next sought to determine whether the effects of Wit were limited to EGF and IL-6 stimulation of STAT3 and/or STAT5 tyrosine phosphorylation."

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"Starting with MDA-MB-468 cells, a human breast cancer cell line where EGF is known to induce STAT3 phosphorylation, we demonstrated as shown in XREF_FIG, that Wit inhibited EGF stimulated tyrosine phosphorylation of STAT3, with an IC 50 of about 1-3muM."

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"In contrast, depletion of Grb2 by RNA interference substantially increases Stat3 tyrosine phosphorylation induced by EGF."

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"XREF_FIG shows that in the absence of Wit, EGF stimulated the tyrosine phosphorylation of both STAT3 and STAT5."

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"In the present study, we report that transient expression of Grb2 specifically down-regulates EGF stimulated tyrosine phosphorylation of Stat3, which leads to a repression of Stat3 transcriptional activity."

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"We further demonstrate that JNK1, activated by its upstream kinase MKK7, negatively regulated the tyrosine phosphorylation and DNA binding and transcriptional activities of Stat3 stimulated by EGF."

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"As expected, the expression of GSTP1 was effectively blocked by GSTP1 siRNA, and GSTP1 siRNA further enhanced the EGF stimulated tyrosine phosphorylation of Stat3 (XREF_FIG)."

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"STAT3 is rapidly tyrosine phosphorylated in response to IL-6, ciliary neurotrophic factor, oncostatin M, leukemia inhibitory factor, IL-11, granulocyte colony stimulation factor and epidermal growth factor."

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"The transient expression of GSTP1 specifically downregulated epidermal growth factor (EGF)-mediated tyrosine phosphorylation of Stat3, and subsequently suppressed the transcriptional activity of Stat3."
EGF leads to the phosphorylation of STAT3 on Y705. 10 / 10
3 | 1 6

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"In addition, neither HIV + exosomes nor EGF induced the phosphorylation of STAT3 at Y705 ( xref , xref ), although these cells displayed basal levels of phosphorylation of STAT3 ( xref )."

"To address this problem, we use quantitative mass spectrometry to analyze dynamic effects of HER2 overexpression on phosphotyrosine signaling in human mammary epithelial cells stimulated by epidermal growth factor (EGF) or heregulin (HRG). [This is from the 'Suplementary Table with Full Data Set\" (http://www.nature.com/msb/journal/v2/n1/suppinfo/msb4100094_S1.html). The cutoff used was a 2.5 fold or greater increase at any of the 5, 10 or 30 minute time points.]"

"To address this problem, we use quantitative mass spectrometry to analyze dynamic effects of HER2 overexpression on phosphotyrosine signaling in human mammary epithelial cells stimulated by epidermal growth factor (EGF) or heregulin (HRG). [This is from the 'Suplementary Table with Full Data Set\" (http://www.nature.com/msb/journal/v2/n1/suppinfo/msb4100094_S1.html). The cutoff used was a 2.5 fold or greater increase at any of the 5, 10 or 30 minute time points.]"

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"KDI1 does not block EGFR’s RTK activity directly but interferes with EGF-induced phosphorylation of Tyr-705 in STAT3 protein [ xref ]."

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"Furthermore, DDIAS knockdown suppressed EGF-induced STAT3 Y705 phosphorylation (Fig. xref ) and inhibited the nuclear translocation of IL-6–mediated pSTAT3 (Fig. xref )."

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"Specifically, constitutive and epidermal growth factor-induced phosphorylation of STAT3 on Y705 was observed only in SCC but not in either immortalized (HaCaT) or normal keratinocyte strains."

"EGF-induced phosphorylation of the tyrosine residues 845, 1068, and 1148 as well as the phosphorylation of tyrosine 317 of p46 Shc. EGF-induced phosphorylation of Stat3 at tyrosine 705"

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"EGF-induced phosphorylation of Stat3 at tyrosine 705 and Stat3-dependent transactivation were also impaired."

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"EGF treatment induced a biphasic STAT3 phosphorylation at Y705 in miR-204 overexpressing cells in the first hours, whereas pY705-STAT3 was barely detectable in control cells."

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"There is evidence showing that STAT3 activation is dependent on Ca2+ signal in breast cancer cells, and phosphorylation of STAT3 at Tyr705 by EGF can be substantially inhibited upon intracellular Ca2+ chelation [ xref ]."
EGF leads to the phosphorylation of STAT3 on S727. 3 / 3
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"Specific inhibition of ERK-1/2 activity blocked EGF- and BK induced STAT-3 activation and Ser 727 phosphorylation."

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"The addition of OSM and EGF induced the synergistic phosphorylation of STAT3 at Ser727 in wild-type astrocytes (XREF_FIG and Supplementary Fig. 5e)."

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"It was observed that inhibition of ERK½ by U0126 in HTR-8/SVneo cells resulted in concomitant inhibition of EGF-induced increase in STAT1 and STAT3 phosphorylation at ser 727 along with inhibition of degradation of total STAT1 (Figs xref and xref )."
EGF leads to the phosphorylation of STAT3 on Y686. 1 / 1
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"To address this problem, we use quantitative mass spectrometry to analyze dynamic effects of HER2 overexpression on phosphotyrosine signaling in human mammary epithelial cells stimulated by epidermal growth factor (EGF) or heregulin (HRG). [This is from the 'Suplementary Table with Full Data Set\" (http://www.nature.com/msb/journal/v2/n1/suppinfo/msb4100094_S1.html). The cutoff used was a 2.5 fold or greater increase at any of the 5, 10 or 30 minute time points.]"
Phosphorylated EGF leads to the phosphorylation of STAT3. 1 / 1
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"TGFbeta1 induced Smad 2/3 phosphorylation and the combination of EGF, LIF and TGFbeta1 synergistically increased STAT3 phosphorylation over single or double cytokine combinations."