Fig. 1.

DNA damage, Chk1 activation, and increased CIP2A expression in AD human brains and AD mouse/cell models. a Representative immunoblots of γH2A.X, 53BP1, Chk1-S345, Chk1-S296, Chk1-S317, Chk1, CIP2A, and β-actin in AD brains. Blots were from different gels in which the same batch of samples was electrophoresed. b The quantitative analysis of the protein levels in a. Non-phosphorylated proteins such as γH2A.X, 53BP1, total Chk1, and CIP2A were normalized to the β-actin levels; phosphorylated Chk1-S345, -S296, and -S317 were normalized to total Chk1 levels. c Representative immunoblots of γH2A.X, 53BP1, Chk1-S345, Chk1-S296, Chk1-S317, Chk1, CIP2A, and β-actin in APP/PS1 mice brains. d The quantitative analysis of the protein levels in c. e Representative immunoblots of γH2A.X, 53BP1, Chk1-S345, Chk1-S296, Chk1-S317, Chk1, CIP2A, and β-actin in primary neurons with 2 µM Aβ treatment for 48 h. f The quantitative analysis of the protein levels in e. g–h Correlation analysis of Chk1-S345 and γH2A.X, Chk1-S345 and CIP2A in e. i The relative mRNA level of CIP2A in primary neurons with 2 µM Aβ treatment for 12 h. All data represent mean ± SEM, n = 5 in (a–b); n = 3 in (c–i) *P < 0.05, **P < 0.01, ***P < 0.001, compared to controls. Statistical analyses details of all data are listed in the supplementary excel sheet