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Fig. 6 | Cell & Bioscience

Fig. 6

From: Post-translational modification of CDK1–STAT3 signaling by fisetin suppresses pancreatic cancer stem cell properties

Fig. 6

STAT3 was interacted and activated by CDK1. a, b The direct interaction and location between STAT3 with CDK1-wild type and mutants were examined by in situ PLA analysis. Top and side views of reconstructed 3D images of confocal micrographs were generated by Imaris software. Red spots represented positive interaction between STAT3 and CDK1. Scale bars 10 μm. Number of positive spots was counted by Imaris software, results were from three independent experiments. *P < 0.05, ns, no significance. c CDK1 interacted with STAT3. Myc-tagged CDK1-WT or K33R/Q mutants were over-expressed in PANC-1 cells. The interaction between CDK1 and STAT3 was determined by immunoprecipitation and western blot analysis. CDK1-WT interacted with STAT3 while CDK1 K33R/Q mutants weakened binding capacity with STAT3 and p-STAT3 (Y705). d, e Immunofluorescence was used to detect the phosphorylation of STAT3 Y705. CDK1-WT not K33R/Q mutants increased levels of p-STAT3 Y705. Scale bars 20 μm. The spots of p-STAT3 were counted by Imaris software, results were from three independent experiments. *P < 0.05, ns, no significance

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