KAT7/HMGN1 signaling epigenetically induces tyrosine phosphorylation-regulated kinase 1A expression to ameliorate insulin resistance in Alzheimer’s disease

Figure 6 KAT7 epigenetically induces dual-specificity tyrosine phosphorylation-regulated kinase-1A expression in a HMGN1 dependent-manner. The insulin-resistant neurons were transfected with siKAT7 or siHMGN1 with or without dual-specificity tyrosine phosphorylation-regulated kinase-1A (DYRK1A) overexpression. A: The protein levels of p-AKT, total AKT, p-GSK3β, total GSK3β, and IRS-1 in neurons were assessed via western blotting; B: Histogram to quantify relative protein expression of pAKT in A; C: Histogram to quantify relative protein expression of pGSK3β in A; D: Histogram to quantify relative protein expression of IRS-1 in A; E: The protein levels of p-AKT, total AKT, p-GSK3β, total GSK3β, and IRS-1 in neurons treated with siHMGN1 and DYRK1A overexpression were assessed via western blotting; F: Histogram to quantify relative protein expression of pAKT in B; G: Histogram to quantify relative protein expression of pGSK3β in B; H: Histogram to quantify relative protein expression of IRS-1 in B. DYRK1A: Dual-specificity tyrosine phosphorylation-regulated kinase-1A.