Fig. 1.

β-Amyloid fibrils stimulate activation of NFκB and multiple MAP kinase pathways in THP-1 cells. THP-1 cells were stimulated in serum-free RPMI with fibrillar Aβ25–35 (60 μm) for increasing times (0–60 min). Cell lysates were resolved by 7.5% SDS-PAGE and Western-blotted with selected antibodies. The p65 (RelA) subunit of NFκB was immunoprecipitated from the stimulated cell lysates and resolved by 7.5% SDS-PAGE and Western-blotted. ERK2 levels were evaluated in parallel as a protein loading control. The antibodies used were 4G10 (anti-phosphotyrosine), anti-phospho-ERK, anti-phospho-p38, anti-phospho-IκBα, anti-IκBα, anti-p65NLS, anti-c-fos, anti-phospho-CREB, and anti-ERK2.