Figure 1From: U1 small nuclear ribonucleoproteins (snRNPs) aggregate in Alzheimer’s disease due to autosomal dominant genetic mutations and trisomy 21U1 snRNPs enriched in PS1 insoluble proteome. (A) Heat map showing quantitative proteomics of frontal cortex from 5 pathology free controls and 6 carriers of pathogenic PS1 mutations (insoluble fraction) demonstrated enrichment (yellow color) of RNA splicing factors and other AD associated proteins in PS1 mutation carriers (FAD-PS1). Log2 of mean of the extracted ion intensities (XIC; normalized protein intensities based on raw signal to noise ratio; Additional file 1: Table S1) in the insoluble fraction from individual cases are shown. (B) Western blot showing insoluble U1-70k in two sporadic (sAD) and two control cases with calnexin loading control. (C) Western blot showing insoluble U1-70k in 6 PS1 mutation carriers with α-tubulin as loading control.Back to article page