Fig 1: Molecular analysis of muscle regulatory proteins in p62−/− and control mice (CON). Panels (a)–(g) are labeled within the figure. (a) Quantitative analysis of protein expression levels in soleus muscle, including total and phosphorylated mTOR (T‐mTOR and P‐mTOR), total and phosphorylated AKT (T‐AKT and P‐AKT), insulin receptor β (IR‐β), glucose transporter 4 (GLUT4), MuRF1, atrogin‐1, and tumor necrosis factor α (TNF‐α). (b) Representative western blot images of protein expression in soleus muscle. β‐actin (37 kDa) was used as a loading control. Predicted molecular weights: mTOR (289 kDa), phospho‐mTOR (289 kDa), AKT (60 kDa), phospho‐AKT (60 kDa), MuRF1 (40 kDa), Atrogin‐1 (42 kDa), IR‐β (95 kDa), GLUT4 (45 kDa), TNF‐α (17 kDa), NBR1 (130 kDa), and GAPDH (37 kDa). (c) Quantitative analysis of the same panel of proteins in gastrocnemius muscle. (d) Representative western blot images of protein expression in gastrocnemius muscle. β‐actin (37 kDa) served as loading control. (e) Representative western blot images of NBR1 in soleus and gastrocnemius muscles, a marker of autophagy dysfunction. (f) Quantitative analysis of NBR1 expression, showing significantly increased levels in soleus muscle of p62−/− mice, suggesting impaired autophagic flux. (g) Ratio of phosphorylated to total AKT in soleus muscle, representing the activation state of this key insulin signaling protein under basal, non‐stimulated condition. All data represent mean ± SD (n = 9 per group). *p < 0.05, significantly different from CON.