Inhibition of p38MAPK-dependent phosphorylation of E2F4 in its T249/T251 motif prevents DNA damage-induced death in N2a-derived neurons
Aina Maria Llabrés Mas, Alberto Garrido García, Vanesa Cano Daganzo, José Maria Frade López · FENS Forum 2024
E2F4 is a transcription factor with a prominent role in cell homeostasis. We have shown that a mutant form of mouse E2F4 (E2F4DN), carrying T249A/T251A mutations, is a multifactorial therapeutic agent against Alzheimer’s disease (AD). Our current hypothesis for the mechanism of action of E2F4DN is that the phosphorylation of the Thr249/Thr251 motif by the stress kinase p38MAPK prevents the homeostatic function of E2F4, while E2F4DN restores it. To test this hypothesis, we have focused on N2a neuroblastoma-derived neurons treated with camptothecin (CPT) to induce DNA damage, as a mechanism of c
ePoster · Neuroscience