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Fig. 3 | Alzheimer's Research & Therapy

Fig. 3

From: Krüppel-like factor 5 accelerates the pathogenesis of Alzheimer’s disease via BACE1-mediated APP processing

Fig. 3

KLF5 regulates the BACE1 expression and promotes amyloidogenic APP processing in HT22 cells. A mRNA level of BACE1 in HT22 cells transfected with KLF5 or the control vector. B Representative Western blots and relative quantification of the protein expression levels of KLF5 and BACE1 in HT22 cells transfected with KLF5 or the control vector. C BACE1 activity (fluorogenic BACE1 activity assay) in HT22 cells transfected with KLF5 or the control vector. D mRNA levels of KLF5 and BACE1 in HT22 cells transfected with KLF5 shRNA or control-shRNA. E Representative Western blots and relative quantification of the protein expression levels of KLF5 and BACE1 in HT22 cells transfected with KLF5 shRNA or control-shRNA. F BACE1 activity (fluorogenic BACE1 activity assay) in HT22 cells transfected with KLF5 shRNA or control-shRNA. G Representative Western blots of the protein expression levels of APP (upper panel) and KLF5 (middle panel) in HT22 cells co-transfected with APPswe and KLF5 or the control vector. H Representative Western blots and relative quantification of the protein expression of APP-CTFβ in HT22 cells co-transfected with APPswe and KLF5 or the control vector. I Levels of Aβ40, Aβ42, and sAPPβ in the medium of HT22 cells co-transfected with APPswe and KLF5 or the control vector. Data are mean ± s.e.m of three separate experiments (*P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001; t-test with parametric data, Mann–Whitney test with nonparametric data, and one-way ANOVA)

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