Fig. 7.

GRP78 deficiency suppresses AKT signaling. a Cardiac myocyte-specific knockout of GRP78 in adult mice led to decreases in AKT and mTOR signaling. GAPDH was used as a loading control. b Quantification to GAPDH of a showed significant suppression in AKT phosphorylation and mTOR activation. N = 6. c GRP78 knockdown by siRNA in NRVMs led to inhibition of AKT signaling and the mTOR pathway. GAPDH was used as a loading control. d Relative quantification to GAPDH of c showed significant reduction of AKT and mTOR signaling by GRP78 knockdown in NRVMs. N = 4–7. *p < 0.05; **p < 0.01; ***p < 0.001