Figure 4
Amyloid beta (Aβ)-induced neurotoxic responses enhance the association of key neuronal proteins with apurinic/apyrimidinic endonuclease 1 (APE1)/redox effector factor-1 (Ref-1). APE1/Ref-1-interacting proteins that are differentially expressed after treatment of PC12 neuronal cells with Aβ (25–35) peptide26 include cytoskeleton elements such as tropomodulin 3 (Tmod3) and the tropomyosin alpha-3 chain; energy metabolism proteins such as pyruvate kinase M2 (PKM2); N-acetyltransferase; sulfotransferase1c; and stress-responsive proteins such as leucine-rich and death domains, anti-NGF 30 and heterogenous nuclear ribonucleoprotein-H1 (hnRNP-H1).
