Control of transferrin expression by β-amyloid through the CP2 transcription factor

摘要: Accumulation of β-amyloid protein (Aβ) is one the most important pathological features Alzheimer’s disease. Although Aβ induces neurodegeneration in cortex and hippocampus through several molecular mechanisms, few studies have evaluated modulation transcription factors during Aβ-induced neurotoxicity. Therefore, this study, we investigated transcriptional activity factor CP2 neuronal damage mediated by (Aβ1–42 Aβ25–35). An unbiased motif search transferrin promoter region showed that binds to promoter, an iron-regulating protein, regulates transcription. Ectopic expression led increased at both mRNA levels, whereas knockdown down-regulated expression. Moreover, trans-activated a reporter gene. electrophoretic mobility shift assay chromatin immunoprecipitation region. Furthermore, binding affinity was regulated Aβ, as Aβ25–35) markedly for promoter. Taken together, these results suggest contributes pathogenesis disease inducing via up-regulating its