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• W2044408038 abstract "The β amyloid (Aβ), the major protein component of brain senile plaques in Alzheimer's disease (AD), causes oxidative stress-inducing DNA damage, resulting in neuronal cell death in AD brain and cultured cortical neurons. It is established that Aβ-induced neurotoxicity occurs through the induction of apoptotic pathways including pro-apoptotic factors, Ataxia telangiectasia mutated (ATM) and p53. The specific signaling pathway, however, mediating this Aβ-induced cellular death has not been completely elucidated. We have previously reported that ATBF1 (AT-motif binding factor 1) is highly expressed in the nucleus of postmitotic neurons and it induces cell cycle arrest associated with neuronal differentiation in the developing brain. Furthermore, the subcellular localization of ATBF1 is regulated by PI3 kinase including ATM. Recently, we found that ATBF1 is highly expressed in the AD brain and APP transgenic mice compared with age-matched control. The aim of this study is to investigate whether ATBF1 plays any role in the pathogenesis of AD brain. Hippocampal specimens were obtained postmortem from patients with histopahologically confirmed AD and control. Primary cortical neurons were established from E17 rats. Apoptotic cells caused by treatment with Aβ (1-42) and etoposide were determined by Caspase-3/7 Activities assay and TUNEL assay. To knock down the endogenous ATBF1, primary cultured neurons were transfected with 50 nM of the synthesized siRNA targeting ATBF1 or with the Stealth RNAi negative control (Invitrogen). We found that ATBF1 expression was up-regulated in the cultured rat cortical neurons treated with different genotoxic compounds (etoposide, homocysteine). It has been reported that these genotoxic agents involved in pathogenesis of AD and induce apoptosis in cultured cortical neurons. Apoptosis induced by Aβ and etoposide in cultured neurons was attenuated by small interfering RNA-mediated knock down of ATBF1. We also found that ionizing irradiation and etoposide induce phospholylation of ATBF1 and that ATBF1 binds to ATM to activate ATM signaling pathways. Our data suggest that ATBF1 expression is enhanced by increased level of Aβ in AD brain and APP transgenic mouse brain, and enhanced level of ATBF1, in turn, activates ATM signaling pathways responsible for the neuronal cell death." @default.
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• W2044408038 date "2009-07-01" @default.
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• W2044408038 title "P2-163: A-beta enhance the ATBF1 expression responsible for the neuronal cell death" @default.
• W2044408038 doi "https://doi.org/10.1016/j.jalz.2009.04.475" @default.
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