IndraLab

"STAT3 is also phosphorylated by ERK1/2 on S727, which enhances its transcriptional activity ( xref , xref )."

"Recently, we have reported dissociation of ethanol potentiation of Ang II stimulated p42/44 MAPK phosphorylation from p42/44 MAPK dependent phosphorylation of serine 727 of STAT3 in hepatocytes ( xref )."

"ERK can also phosphorylate STAT3 at Ser727 [ xref ], but we observed no significant changes in phosphorylated STAT3 levels in our study."

"It is well known that the STAT3 Ser727 residue is phosphorylated mainly by Erk1/2, p38 MAPK, JNK and mTOR [ xref - xref ]."

"Based on our finding that ERK phosphorylates STAT3 on Ser727, we investigated whether Tyr705 phosphorylation of STAT3 is stimulated by galectin-1."

"STAT3 can also be phosphorylated at Ser727 by extracellular signal-regulated kinase (ERK), which augments the effect of Tyr705 phosphorylation [ xref ]."

"Besides Tyr 705 phosphorylation, STAT3 can also be phosphorylated on Ser 727 by extracellular signal regulated kinase (ERK) in ESCs."

"As mentioned above, Erk1/2 phosphorylates Stat3 at Ser 727 residue, whereas Src phosphorylates Stat3 at Tyr 705 residue, the phosphorylation at both residues being necessary for Stat3 activation and subsequent dimerization."

"On the contrary, inhibition of ERK pathway at the level of MEK, decreased phosphorylation of STAT3 on Ser727, but had no effect on phosphorylation of STAT3 on Tyr705, despite leptin or NaW treatment."

"STAT3 can be phosphorylated at Ser727 by mTORC1 or ERK1/2 [ xref , xref ]."

"Phosphorylation of STAT3 activates the ERK and Akt pathways, which also promote phosphorylation of STAT3."

"Conversely, while the MEK1/2 inhibitor U0126 and the STAT3 inhibitor WP1066 both inhibited ERK and STAT3 phosphorylation, neither affected IDO expression."

"It is now obvious that serine phosphorylation of STAT-3 by ERKs, p38, or Jun-N-terminal kinase [36] is required for maximal transcriptional activation of STAT-3 [37,38] , a situation which has also[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"In this study, trametinib, a mitogen activated protein and extracellular signal regulated kinase kinase (MEK) inhibitor, reduced the p-ERK level and significantly increased signal transducer and activator of transcription 3 (STAT3) phosphorylation in GC cells, resulting in reduced sensitivity to trametinib."

"Phosphorylation of STAT3 and CREB can be directly or indirectly mediated by both MAPK p38 and ERK1/2 XREF_BIBR, XREF_BIBR."

"Finally, ERK1/2 inhibition in naive mice decreased KIM-1 mRNA and nuclear STAT3 phosphorylation in the cortex, indicating homeostatic regulation of KIM-1."

"It was reported that ERK phosphorylates and activates both STAT3 and Elk‐1 40, 41."

"In FPR2-expressing RBL-2H3, cells the stimulation of FPR2 by WKYMVm induces ERKs phosphorylation and serine phosphorylation of STAT3 in a PTX-sensitive manner."

"Both Akt and ERK are known to induce STAT3 phosphorylation independently of cytokine stimulation (Zhao et al., 2004)."

"Specific inhibitors of p38 (SB203580), ERK (PD98059), and JNK (SP600125) inhibited MK1-EPS-induced HUVEC proliferation, tube formation, and cell migration, and partially attenuated MKI-EPS-induced expression of p21 and ICAM1, and STAT3 phosphorylation."

"Furthermore, our study reveals that PDGF-BB- and bFGF induced proliferation does not affect the osteogenic differentiation potential of hBMMSCs.All of the three GFs activated the hBMMSC ERK1/2 pathway[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"These results strongly suggest that STAT3 serine phosphorylation upon BMP2 and BMP4 stimulation is distinctively mediated by mTOR and ERK1/2, respectively, in human MSCs.Next, we sought to corroborate[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"Here, we show that STAT3 serine phosphorylation is induced by ERK and JNK as a downstream effect of FGFR signaling and it does not require over-expression of FGFRs."

"Notably, inhibition of the ERK1/2 pathway greatly decreased STAT3 serine phosphorylation in response to PDGF-BB, indicating that ERK1/2 mediate PDGF-BB-induced STAT3 serine phosphorylation."

"STAT1 serine phosphorylation was perturbed by inhibition of ERK and p38 pathways, whereas only inhibition of ERK activation blocked STAT3 serine phosphorylation in response to EPO."

"Furthermore, stimulation with SCF and PMA, previously shown to induce phosphorylation of ERK and subsequent serine phosphorylation of STAT3, also resulted in the activation of MSK1 (data not shown)."

"We also found that WKYMVm stimulated extracellular signal regulated kinase (ERK), and that ERK activity is required for STAT3 serine phosphorylation."

"To determine whether ERK1/2 also mediate PDGF-BB-induced STAT3 serine phosphorylation, PD98059, a specific inhibitor of MEK and, therefore, its downstream targets, ERK1/2, was employed (Dudley et al.,[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"Interestingly, the exact opposite were observed using BMP4; ERK1/2 inhibition prevented STAT3 serine phosphorylation, whereas mTOR obstruction did not."

"STAT3 serine phosphorylation by ERK dependent and -independent pathways negatively modulates its tyrosine phosphorylation."

"Interestingly, serine phosphorylation of STAT3 by ERK has been reported to negatively modulate STAT3 tyrosine phosphorylation and activity [250, 251], while other studies implicate the MEK/ERK cascade in positively mediating STAT3 activity [252–254]."

"Furthermore, our study reveals that PDGF-BB- and bFGF induced proliferation does not affect the osteogenic differentiation potential of hBMMSCs.All of the three GFs activated the hBMMSC ERK1/2 pathway[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"Furthermore, PDGF-BB-induced STAT3 tyrosine and serine phosphorylation in hBMMSCs are directly mediated by JAK2 and ERK1/2, respectively."

"Although previous studies clearly demonstrated serine phosphorylation of STAT3 regulates ERK, the current results indicate that ERK may also phosphorylate tyrosine on STAT3."

"These results suggest that JAK2 and ERK may mediate tyrosine and serine phosphorylation of STAT3 induced by histamine, respectively, and that both phosphorylations may be required for the activation o[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"ERK1/2 specifically phosphorylates STAT3 at serine 727, which negatively modulates STAT3 tyrosine phosphorylation [XREF_BIBR]."

"Interestingly, serine phosphorylation of STAT3 by ERK has been reported to negatively modulate STAT3 tyrosine phosphorylation and activity [XREF_BIBR, XREF_BIBR], while other studies implicate the MEK and ERK cascade in positively mediating STAT3 activity [XREF_BIBR - XREF_BIBR]."

"Inhibition of ERK activation by AZD6244 leads to derepression of STAT3, as ERK mediated STAT3 (S727) phosphorylation negatively modulates STAT3 tyrosine phosphorylation at Y705 which is required for dimer formation, nuclear translocation, and DNA binding activity of this transcriptional regulator."

"Inhibition of MEK and ERK with U0126 totally blocked the phosphorylation of STAT3 (Tyr705 and Ser727) but increased the phosphorylation of CREB and ATF1 (XREF_FIG)."

"The activity of ERK1/2 in leptin and OB3 co-treated cells was inhibited by PD98059 and further reflected in leptin induced phosphorylation of STAT3 Tyr 705 and ERalpha."

"In this study, we examined the effect of BARD on oxidative stress signalling by assessing the stress activated proteins including phosphorylated protein kinase B (pAkt), phosphorylated extracellular signal regulated kinase (pERK), phosphorylated signal transducer and activator of transcription 3 (pSTAT3), and phosphorylated c-Jun N-terminal kinase (pJNK) in mesenteric adipose tissue."

"In this study, we examined the effect of BARD on oxidative stress signalling by assessing the stress activated proteins including phosphorylated protein kinase B (pAkt), phosphorylated extracellular signal regulated kinase (pERK), phosphorylated signal transducer and activator of transcription 3 (pSTAT3), and phosphorylated c-Jun N-terminal kinase (pJNK) in mesenteric adipose tissue."

"Studies have shown that phosphorylation of ERK can drive phosphorylation of STAT3 [21]."

"enhanced proliferation of KMS-11. bFGF but not IL-6 stimu- lation induces the phosphorylation of Ser727 in STAT3, and a selective MEK1/2 inhibitor abolishes the serine- but not tyrosine-phosphorylation of STAT3 in response to bFGF and IL-6 stimulations, supportingthe notion that two independent signaling pathways converge on STAT3 to regulate its func- tion in the cell. Thus, the bFGF-induced activation of ERK1/ 2 pathway is involved in the phosphorylation of the critical serine residue of STAT3 "

"Figure 5. This is a figure in the review representing the cross talk between FGFR3 and IL6 signaling in multiple myeloma cell line KH11; the legend is as follows: Fig. 5. Enhanced proliferation of myeloma cells by interleu- kin- 6 cooperatingwith FGFR3-mediated signals. IL- 6 and FGF induce the distinct intracellular signaling pathways in myeloma cells carryingt(4 ;14)(p16. 3 ;q32) that ectopically express FGFR3. FGF and IL- 6 activate ERK1/ 2, PI- 3 kinase and STAT3, respectively. The serine phosphorylation of STAT3 via the FGF- induced ERK1/ 2 activation contributes to the full activation of STAT3, leadingto the expression of c-myc and bcl- 2 genes and cell proliferation 91 .FRS:FGF receptor substrate."