Fig. 5
ACTN1 promotes GSK-3β degradation by enhancing its interaction with MYH9. A GSK-3β expression in ACTN1-depleted cells and control cells. B GSK-3β levels in ACTN1-overexpressing cells and control cells. C-D Influence of ACTN1 upregulation on GSK-3β expression in HNSCC cells with or without the proteasome inhibitor, MG132. E–F Degradation rate of GSK-3β in ACTN1-depleted HNSCC cells compared to control cells. G-H Effect of ACTN1 overexpression on the half-life of GSK-3β in HNSCC cells. I-J Interaction between ACTN1 and MYH9 in HNSCC cells as demonstrated by endogenous and exogenous Co-IP assays. K Schematic representation of MYH9 domains. L-N Interactions between MYH9 domains and ACTN1 in SCC-1cisR cells as revealed by Co-IP experiments. O Schematic representation of ACTN1 domains. P Interactions between ACTN1 domains and MYH9 in SCC-1 cells as illustrated by Co-IP experiments. Q GSK-3β expression in HNSCC cells subjected to indicated treatments. R-S Effects of ACTN1 overexpression or depletion on the interaction between MYH9 and GSK-3β in HNSCC cells. T Impact of ACTN1 depletion on the ubiquitination level of GSK-3β in HNSCC cells. U Ubiquitination level of GSK-3β in HNSCC cells subjected to specified modifications