Fig. 4: Accumulated NEU1 promotes cardiac injury by inhibiting AKT signaling.
From: Sotorasib-impaired degradation of NEU1 contributes to cardiac injury by inhibiting AKT signaling
CCC-HEH-2 cells were treated with 20 μM sotorasib for 0, 12, 24, 36, and 48 h and exposed to different concentrations of 0, 10, 15, or 20 μM sotorasib for 48 h. A, B Expression levels of AKT1 and p-AKT Ser473 protein in CCC-HEH-2 cells (n = 3). C CCC-HEH-2 cells transfected with NC and NEU1#1 knockdown were treated with sotorasib for 48 h. Expression levels of AKT1 and p-AKT Ser473 protein in CCC-HEH-2 cells (n = 3). D CCC-HEH-2 cells were treated with 20 μM sotorasib for 0, 12, 24, 36, and 48 h and exposed to different concentrations of 0, 10, 15, or 20 μM sotorasib for 48 h. Expression levels of PGC-1α protein in CCC-HEH-2 cells (n = 3). E CCC-HEH-2 cells transfected with NC and NEU1#1 knockdown were treated with sotorasib for 48 h. Expression levels of PGC-1α protein in CCC-HEH-2 cells (n = 3). F CCC-HEH-2 cells were treated with 20 μM sotorasib for 0, 12, 24, 36, and 48 h and exposed to different concentrations of 0, 10, 15, or 20 μM sotorasib for 48 h. Expression levels of p-AMPK Thr172 protein in CCC-HEH-2 cells (n = 3). G CCC-HEH-2 cells transfected with NC and NEU1#1 knockdown were treated with sotorasib for 48 h. Expression levels of p-AMPK Thr172 protein in CCC-HEH-2 cells (n = 3). Data expressed as mean ± SD, ***, p < 0.0001, **, p < 0.01, *, p < 0.05 (vs. Vehicle), #, p < 0.05 (vs. sotorasib), ns, no significance.
