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A, B
Overexpression of hTau in HEK293 cells for 48 h increased the activity‐dependent phosphorylation of JAK2, JNK1, and ERK1 compared with the empty vector control (Ctrl) measured by Western blotting (n = 3, Student's t‐test).
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C–F
Pharmacological inhibition of ERK1 (C, D) or JNK1 (E, F) for 24 h did not significantly affect the hTau‐induced STAT1 phosphorylation at pY‐STAT1 (Tyr701) in total extracts (C, E) and the nuclear fraction (D, F) measured by Western blotting (n = 3). The alteration of pS‐STAT1 (Ser727) confirms the efficacy of JNK1 inhibitors.
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G–J
Pharmacological inhibition of JAK2 (G, H) or knockdown of JAK2 by siRNA (I, J) abolished hTau‐induced STAT1 phosphorylation at Tyr701 in total extracts (G, I) and the nuclear fraction (H, J) (n = 3).
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K, L
The phosphorylated JAK2 level increased in the hippocampus of 12‐month‐old hTau transgenic mice (K) and the hippocampus of C57 mice infected with AAV‐hTau (1.13 × 1013 v.g./ml) (L) (n = 4, Mann–Whitney test).
Data information: Data were presented as mean ± SD, *
P < 0.05 vs Ctrl, eGFP, or WT.
Source data are available online for this figure.
