Figure 3.

Loss of NCLX increases tau-pathology

(A) Representative western blots of soluble total tau (HT7), and phosphorylated tau at residues S202/T205 (AT8), T231/S235 (AT180), T181 (AT270), and S396 (PHF13) in cortex homogenates of 16-month-old mice, n = 3 for all groups.

(B–E) Densitometric analysis of western blots shown in Figure 3A expressed as fold-change versus Camk2a-Cre con. Corrected to a loading control tubulin.

(F) Representative immunohistochemical staining for total tau (HT7) and phospho-tau T231/S235 (AT180) in hippocampus of NCLX-nKO and control mice; scale bar = 50 μM.

(G and H) Quantification of the integrated optical density area of HT7 and AT180 immunoreactivity, n = 4 for all groups. All data presented as mean ± SEM; ∗∗p<0.01, ∗p<0.05; two-tailed, unpaired t-test.