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Fig. 2 | Acta Neuropathologica Communications

Fig. 2

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

Fig. 2

Modules that correlate to Grn deficiency and age highlight dysregulation of proteins involved in the lysosome, inflammation, and neuronal synaptic function. a–c Box plots illustrate eigenprotein values for modules (M7, M16, and M6 red) that are upregulated in 3- or 19-month-old Grn−/− mice compared to Grn+/+ mice. d–f Box plots of M5, M3 and M19 modules that have decreased eigenprotein values in Grn−/− versus Grn+/+ in 19-month-old mice. Values were analyzed by two-way ANOVA. Gene ontology (GO) enrichment analysis, calculated using GO Elite v1.2.5, of proteins in modules, highlights proteins involved in: g immune effector process, glycoprotein-binding, lysosome (M7), h protein transport, hydrolase activity, lysosome (M16), i oxidoreductase activity, regulation of NF kappa B cascade, lysosome (M6), j glutamate signaling, postsynaptic density, neuron spice and dendrite (M5), k regulation of neurotransmitter secretion, voltage-gated potassium channel activity, cytoplasmic microtubule (M3), i regulation of creation, synaptic membrane and synapses (M19). Light-green bars: biological process, light-blue bars: molecular function, brown-bars: cellular component

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Acta Neuropathologica Communications

ISSN: 2051-5960

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