The WNT/β-catenin pathway was stimulated with mouse Recombinant WNT3a (Peprotech, NJ, USA) at a final concentration of 100 ng/ml. β-catenin transcriptional activity was inhibited by treating cells with iCRT14 (Santa Cruz, CA, USA) at a final concentration of 10 μM. c-Met signalling was stimulated with recombinant human HGF (R&D Systems) at a final concentration of 75 nM, whilst it was inhibited with Capmatinib (Biozol Diagnostica, Eching, Germany) at a final concentration of 2 nM. c-Met and EGFR signalling were concomitantly stimulated with recombinant human EGF (Corning, NY, USA) at a final concentration of 20 nM. Downstream signalling was inhibited with Erlotinib at a final concentration of 5 μM. Recombinant WNT3a, HGF, and EGF were diluted in 0.1% BSA in PBS, which was therefore used as a control in all experiments and is indicated with the “unstimulated” label in respective figures. iCRT-14 and Capmatinib were diluted in DMSO, whilst Erlotinib was diluted in PBS. Thus, the respective vehicle controls (veh. ctrl) were used in the experiments.
Recombinant wnt3a
Manufactured by Corning
Sourced in United States
Recombinant WNT3a is a purified protein produced in mammalian cells. It is a member of the Wnt family of signaling proteins, which play crucial roles in various cellular processes. This product provides a reliable source of WNT3a for use in cell culture and research applications.
Automatically generated - may contain errors
2 protocols using recombinant wnt3a
1
Modulating Signaling Pathways in Cells
2
Modulating WNT, c-Met, and EGFR Signaling
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The WNT/β-catenin pathway was stimulated with mouse Recombinant WNT3a (Peprotech, NJ, USA) at a final concentration of 100 ng/ml. β-catenin transcriptional activity was inhibited by treating cells with iCRT14 (Santa Cruz, CA, USA) at a final concentration of 10 µM. c-Met signalling was stimulated with recombinant human HGF (R&D Systems) at a final concentration of 75 nM, whilst it was inhibited with Capmatinib (Biozol Diagnostica, Eching, Germany) at a final concentration of 2 nM. c-Met and EGFR signalling were concomitantly stimulated with recombinant human EGF (Corning, NY, USA) at a final concentration of 20 nM. Downstream signalling was inhibited with Erlotinib at a final concentration of 5 µM. Recombinant WNT3a, HGF, and EGF were diluted in 0.1% BSA in PBS, which was therefore used as a control in all experiments and is indicated with the "unstimulated" label in respective figures. iCRT-14 and Capmatinib were diluted in DMSO, whilst Erlotinib was diluted in PBS. Thus, the respective vehicle controls (veh. ctrl) were used in the experiments.
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