IndraLab
Statements
sparser
"We found that B6 had dose-dependent but differential inhibitory effects on the IL-6-induced STAT3 Tyr705 phosphorylation, IFN-γ-induced STAT1 Tyr701 phosphorylation (Fig. xref ) and IFN-α-induced phosphorylation of both STAT1 and STAT3 (Fig. xref ), which was consistent with the luciferase assay results."
sparser
"It has been shown that IL-6-induced JAK-STAT3 signaling pathway activation plays important roles in endothelial cell activation [ xref ] that is mainly mediated by IL-6-induced Tyr705 phosphorylation in STAT3 [ xref ], which resembles our data on B7-H4 regulation by GM-CSF-induced Tyr705 phosphorylation of STAT3 in neutrophils."
"Phosphorylation of a tyrosine residue at 705 in STAT3 is observed in KMS-11 in response to IL-6. In contrast, bFGF induces the activation of ERK1/2 and PI-3 kinase. These results indicate that IL-6 and bFGF activate the distinct intra- cellular signaling pathways, and both the ERK1/2 and PI-3 kinase pathways activated by bFGF are necessary for the enhanced proliferation of KMS-11. "
reach
"IL-6 strongly induced STAT3 phosphorylation at Y705 but not S727 and was inhibited by WFA after only 2 hours of incubation (XREF_FIG); however, total STAT3 levels were reduced after exposure of cells to WFA for more than 4 hours, suggesting that WFA also downregulates STAT3 protein if cells are exposed to the drug for longer time periods."
reach
"When applied together with sIL-6R, very low concentrations of IL-6 (i.e. 1ng/ml) were sufficient to induce STAT3 Tyr705 phosphorylation (Additional file 3 : Figure S3), while higher concentrations (i.e. 50ng/ml) were required to induce similar degree of phosphorylation when IL-6 is added without sIL-6R."
reach
"Both autocrine and paracrine IL-6 can lead to constitutive phosphorylation of STAT3 at Tyr705 and Ser727 residues; IL-6 from paracrine sources (such as cancer-associated myeloid cells or fibroblasts) could induce autocrine IL-6 production and STAT3 phosphorylation in tumor cells (9)."
sparser
"In our study, we showed that treatment with LPS or IL-6 alone markedly increased the phosphorylation of STAT3 at Tyr 705 and that CCM111 robustly decreased the phosphorylation of STAT3 at Tyr 705 in a dose- and time-dependent manner in macrophage cells or epithelial cells (Figs xref and xref )."
sparser
"IL-6 strongly induced STAT3 phosphorylation at Y705 but not S727 and was inhibited by WFA after only 2 hours of incubation ( xref ); however, total STAT3 levels were reduced after exposure of cells to WFA for more than 4 hours, suggesting that WFA also downregulates STAT3 protein if cells are exposed to the drug for longer time periods."
sparser
"Whereas IL-6 induced STAT3-Tyr705 phosphorylation within a few minutes, the stimulation of the BCR with anti-immunoglobulin M (IgM) antibodies required a few hours, since it involves the transcriptional activity of NF-κB. Remarkably, prolonged incubation with anti-IgM antibodies induces transcription and secretion of IL-6, further promoting the phosphorylation of STAT3 on tyrosine residues."