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Developing master keys to brain pathology, cancer and aging from the structural biology of proteins controlling reactive oxygen species and DNA repair

Academic Article
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Overview

authors

  • Perry, J. J. P.
  • Fan, L.
  • Tainer, John

publication date

  • April 2007

journal

  • Neuroscience  Journal

abstract

  • This review is focused on proteins with key roles in pathways controlling either reactive oxygen species or DNA damage responses, both of which are essential for preserving the nervous system. An imbalance of reactive oxygen species or inappropriate DNA damage response likely causes mutational or cytotoxic outcomes, which may lead to cancer and/or aging phenotypes. Moreover, individuals with hereditary disorders in proteins of these cellular pathways have significant neurological abnormalities. Mutations in a superoxide dismutase, which removes oxygen free radicals, may cause the neurodegenerative disease amyotrophic lateral sclerosis. Additionally, DNA repair disorders that affect the brain to various extents include ataxia-telangiectasia-like disorder, Cockayne syndrome or Werner syndrome. Here, we highlight recent advances gained through structural biochemistry studies on enzymes linked to these disorders and other related enzymes acting within the same cellular pathways. We describe the current understanding of how these vital proteins coordinate chemical steps and integrate cellular signaling and response events. Significantly, these structural studies may provide a set of master keys to developing a unified understanding of the survival mechanisms utilized after insults by reactive oxygen species and genotoxic agents, and also provide a basis for developing an informed intervention in brain tumor and neurodegenerative disease progression.

subject areas

  • Aging
  • Animals
  • Binding Sites
  • Brain Diseases
  • Brain Neoplasms
  • DNA Damage
  • DNA Repair
  • Enzymes
  • Humans
  • Molecular Structure
  • Reactive Oxygen Species
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Research

keywords

  • Werner syndrome
  • amyotrophic lateral sclerosis
  • ataxia-telangiectasia-like disorder
  • nitric oxide synthase
  • superoxide dismutase
  • xeroderma pigmentosum
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Identity

PubMed Central ID

  • PMC1904427

International Standard Serial Number (ISSN)

  • 0306-4522

Digital Object Identifier (DOI)

  • 10.1016/j.neuroscience.2006.10.045

PubMed ID

  • 17174478
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Additional Document Info

start page

  • 1280

end page

  • 1299

volume

  • 145

issue

  • 4

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