Journal: JCI Insight
Article Title: Loss of O-GlcNAcylation modulates mTORC1 and autophagy in β cells, driving diabetes 2 progression
doi: 10.1172/jci.insight.183033
Figure Lengend Snippet: ( A – C ) Representative immunoblot and analysis of TSC2, pS6 S240, and S6 from control, βOGT-KO, βOGT/TSC2-KO, and βTSC2-KO islets ( n = 4–5). ( D – H ) Nonfasted blood glucose over time, i.p. glucose tolerance (glucose 2 g/kg i.p.), and insulin tolerance test (insulin 0.75U/kg i.p.) from male and female control, βOGT-KO, βOGT/TSC2-KO, and βTSC2-KO mice ( n = 3–8). ( I ) In vivo GSIS assay from male control, βOGT-KO, and βOGT/TSC2-KO mice ( n = 4–7). * P ≤ 0.05, Ctrl versus βOGT-KO or βOGT/TSC2-KO, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical analysis by 1-way ( B and C , AUC for E – H ) and 2-way ANOVA ( D and I ).
Article Snippet: Primary antibodies (TSC2 [4308; Cell Signaling Technology], pS6 S240 [5364; Cell Signaling Technology], S6 [sc-74459; Santa Cruz Biotechnology Inc.], RL2 [ab2739; Abcam], OGT [24083; Cell Signaling Technology], OGA [SAB4200267; MilliporeSigma], mTOR [2983; Cell Signaling Technology], Actin [4967; Cell Signaling Technology], Vinculin [E1E9V; Cell Signaling Technology], Tubulin [2146; Cell Signaling Technology], LC3B [3868; Cell Signaling Technology], p62 [5114; Cell Signaling Technology]) were applied, followed by horseradish peroxidase–conjugated secondary antibodies.
Techniques: Western Blot, Control, In Vivo