The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
ATM-mediated transcriptional elevation of prion in response to copper-induced oxidative stress.
Kefeng Qin; Lili Zhao; Richard D Ash; William F McDonough; Richard Y Zhao (Profiled Author: Richard Y Zhao)
Departments of Pathology and Microbiology-Immunology and Institute of Human Virology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
The Journal of biological chemistry 2009;284(7):4582-93.
Increasing evidence suggests that the cellular prion protein (PrP(C)) plays a protective role in response to oxidative stress, but the molecular mechanism is unclear. Here, we demonstrate that murine neuro-2a and human HeLa cells rapidly respond to an increase of intracellular copper concentration by up-regulating ataxia-telangiectasia mutated (ATM)-mediated transcription of PrP(C). Copper stimulation activates ATM by phosphorylation at Ser-1981, which leads to phosphorylation of p53 at Ser-15 and the initiation of the mitogen-activated protein kinase kinase/extracellular-related kinases/extracellular-related kinases (MEK/ERK)/Sp1 pathway. As results, Sp1 and p53 bind to the PrP promoter, leading to increase PrP(C) expression. Elevated PrP(C) correlates with reduction of intracellular copper concentration and suppression of Cu(II)-induced accumulation of reactive oxygen species and cell death. Depletion of PrP(C), ATM, p53, and/or Sp1 further demonstrates that ATM is a key regulatory protein to promote activation of p53 and Sp1 leading to PrP(C) elevation, which is required to reduce Cu(II) toxic effects and may play an important role in modulation of intracellular copper concentration.
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