Additional file 1 of p85S6K sustains synaptic GluA1 to ameliorate cognitive deficits in Alzheimer’s disease

Additional file 1. Table S1: Information of brain donors in this study. Fig. S1: The expression pattern of S6K1 in HEK293 cells and neurons. Fig. S2: The quantification of PSD95 and synaptophysin in fractions and the validation of p70S6K antibodies. Fig. S3: Knockdown of p85S6K efficiently reduces p85S6K in PSD-1 and does not affect the locomotor activity and anxiety-like behavior. Fig. S4: p85S6K cannot be immunoprecipitated with GluA1 with little expression of AKAP79 in HEK293 cells. Fig. S5: p85S6K does not interfere with the interaction between GluA1 and PKA. Fig. S6: The immunoblots of p85S6K/p70S6K and phosphorylated form in remaining human temporal cortex samples related to Fig. 5a. Fig. S7: p85S6K expression in P2 pellets of cortex of APP/PS1 mice. Fig. S8: p85S6K expression is decreased in PSD-1 of cortex of 5×FAD mice. Fig. S9: PSD95 expression is not altered in AD brains. Fig. S10: Overexpression of p85S6K does not affect the locomotor activity and anxiety-like behavior. Fig. S11: Upregulation of p85S6K does not enhance the spatial learning and spine density in S845A mice. Fig. S12: The NLS predicted in p85S6K by www.csbio.sjtu.edu.cn/bioinf/INSP/ . Fig. S13: The expression of GluA1 and its phosphorylation at Ser845 are reduced in P2 pellets from fractionation of cortex of 7-month old 5×FAD and 9-month old APP/PS1 mice.