Fig. 5: TTC36 depletion destabilizes c-Myc by attenuating the interaction between SET and PPP2R1A. | Cell Death & Disease

Fig. 5: TTC36 depletion destabilizes c-Myc by attenuating the interaction between SET and PPP2R1A.

From: TTC36 promotes proliferation and drug resistance in hepatocellular carcinoma cells by inhibiting c-Myc degradation

Fig. 5: TTC36 depletion destabilizes c-Myc by attenuating the interaction between SET and PPP2R1A.

A LO2 cell was transfected with the specified plasmids, and GFP magnetic beads facilitated immunoprecipitation. Subsequent immunoblotting analysis utilized the respective primary antibodies. B, C LO2 cells with or without TTC36 knockout underwent treatment according to indicated conditions, followed by immunoblotting analysis with corresponding primary antibodies after Immunoprecipitation using GFP magnetic beads. D, E Based on the knockdown of TTC36 transfected in PLC/PRF/5 cells and HepG2 cells, PP2A inhibitor or si-PPP2R1A was used to observe changes in downstream target proteins. Western blot analysis was performed using the corresponding antibodies in the figure, with β-Actin protein as an internal control. F LO2 cell, concomitantly overexpressing His-Ub and Flag-c-Myc, experienced diverse treatment conditions as illustrated in the figure. Preceding cell harvesting with guanidine hydrochloride lysis buffer, immunoprecipitation was performed using 30 μL of FLAG affinity beads, followed by immunoblotting with the indicated antibodies.

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