Skip to main content
. 2018 May 4;9:1800. doi: 10.1038/s41467-018-04238-0

Fig. 2.

Fig. 2

Prevention of Aβ accumulation in 6-month-old App 3′-UTR deleted NL-G-F mice. a Aβ pathology in 6-month-old NL-G-F ΔUTR mouse brains, as well as unedited control NL-G-F brains. Scale bar: 1 mm. b Negative correlation between Aβ accumulation and genome editing efficiency in NL-G-F ΔUTR mouse brains (n = 13). c Positive correlation between normalized APP protein expression and genome editing efficiency in NL-G-F ΔUTR mouse brains (n = 13). Western blotting was performed using an antibody against N terminus of APP protein. dg Negative correlation between normalized Aβ levels and deletion efficiency in 6-month-old NL-G-F ΔUTR mouse brains (n = 13). Aβ40 and Aβ42 levels in both the Tris-HCl-buffered saline (TS) and GuHCl fractions were quantified by ELISA. h Strategy of CRISPR/Cas9-mediated NL-G-F Δ400. Positions of targeting sgRNAs are shown by scissors. i Negative correlation between Aβ levels and deletion efficiency in female NL-G-F Δ400 mouse brains (n = 5). j Positive correlation between normalized APP protein expression and genome editing efficiency in NL-G-F Δ400 mouse brains (n = 11)