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Ill-Raga G, Tajes M, Busquets-García A, Ramos-Fernández E, Vargas LM, Bosch-Morató M, Guivernau B, Valls-Comamala V, Eraso-Pichot A, Guix FX, Fandos C, Rosen MD, Rabinowitz MH, Maldonado R, Alvarez AR, Ozaita A, Muñoz FJ

Physiological Control of Nitric Oxide in Neuronal BACE1 Translation by Heme-Regulated eIF2α Kinase HRI Induces Synaptogenesis.

Antioxid. Redox Signal.. 2015 May;22(15):1295-307, PMID: 25706765

Hippocampus is the brain center for memory formation, a process that requires synaptogenesis. However, hippocampus is dramatically compromised in Alzheimer's disease due to the accumulation of amyloid β-peptide, whose production is initiated by β-site APP Cleaving Enzyme 1 (BACE1). It is known that pathological stressors activate BACE1 translation through the phosphorylation of the eukaryotic initiation factor-2α (eIF2α) by GCN2, PERK, or PKR kinases, leading to amyloidogenesis. However, BACE1 physiological regulation is still unclear. Since nitric oxide (NO) participates directly in hippocampal glutamatergic signaling, we investigated the neuronal role of the heme-regulated eukaryotic initiation factor eIF2α kinase (HRI), which can bind NO by a heme group, in BACE1 translation and its physiological consequences.


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