Figure 6
From: Deletion of IRE1α in podocytes exacerbates diabetic nephropathy in mice

Deletion of IRE1α in podocytes attenuates the UPR and autophagy in diabetic nephropathy. (a) Glomerular lysates were immunoblotted with antibodies as indicated (representative immunoblots). (b) Signals were quantified by densitometry (values are normalized to the expression of β-actin). The ER chaperones, GRP94 and MANF, as well as LC3-II and total LC3 were increased significantly in diabetic (STZ-treated) control, but not diabetic IRE1α KO mice. p62 was increased in diabetic IRE1α KO mice compared to untreated KO. N = 4 mice in control, 6 in KO, 6 in Ctrl STZ and 6 in KO STZ groups (ANOVA). *P < 0.05, **P < 0.01, ***P < 0.001. The uncropped immunoblots are presented in Supplementary Fig. 9.