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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Network analysis of the progranulin-deficient mouse brain proteome reveals pathogenic mechanisms shared in human frontotemporal dementia caused by GRN mutations

Fig. 3

The lysosomal proteins, cathepsin D (Cat D) and Cathepsin Z (Cat Z), are elevated in Grn−/− mouse brains. a Images of immunoblots of lysates of Grn+/+ and Grn−/− mouse brains at 3- (n = 4) and 18- (n = 4) months of age probed for Cat (33 kDa), pro Cat D (~ 48 kDa) and the mature heavy chain of Cat D (~ 33 kDa). Alpha-tubulin used as a loading control. bd Fold change of signal intensity determined by comparing the 3-month-old Grn+/+ group mean signal intensity measurement value of Cat Z and Cat D bands from (a) and normalized to total protein signal of blot. f Immunohistochemistry staining of Cat D in 19-month-old Grn+/+ and Grn−/− mouse brains. Region specific Cat D expression in the cortex (I, VII), hippocampus (II, VIII), corpus callosum (III, IX), striatum (IV, X), thalamus (V, XI) and hypothalamus (VI, XII). g Region specific Cat Z expression in the cortex (I, VI), corpus callosum (II, VII), striatum (III, VIII), thalamus (VI, IX), and hypothalamus (V, X) of 19-month-old Grn+/+ and Grn−/− mouse brains. Scale bars (1 nm to 100 µm) are labeled in images and quantitative data shown as mean ± SEM, p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001

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