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Int J Clin Exp Pathol 2011;4(3):xxx-xxx

Review Article
Nuclear transport, oxidative stress, and neurodegeneration

Vivek P. Patel, Charleen T. Chu

Center for Neuroscience at the University of Pittsburgh1; Department of Pathology, Division of Neuropathology2, University of Pittsburgh School
of Medicine, Pittsburgh, PA, USA

Received February 22, 2011; accepted February 27, 2011; Epub February 28, 2011; published March 31, 2011

Abstract: Trafficking of transcription factors between the cytoplasm and the nucleus is an essential aspect of signal transduction, which is
particularly challenging in neurons due to their highly polarized structure.  Disruption in the subcellular localization of many proteins, including
transcription factors, is observed in affected neurons of human neurodegenerative diseases.  In these diseases, there is also growing
evidence supporting alterations in nuclear transport as potential mechanisms underlying the observed mislocalization of proteins.  Oxidative
stress, which plays a key pathogenic role in these diseases, has also been associated with significant alterations in nuclear transport.  After
providing an overview of the major nuclear import and export pathways and discussing the impact of oxidative injury on nuclear trafficking of
proteins, this review synthesizes emerging evidence for altered nuclear transport as a possible mechanism in the pathogenesis of
neurodegenerative diseases. Potential strategies to overcome such deficits are also discussed. (IJCEP1102006).

Keywords: Nuclear transport, nuclear pore complex, oxidative stress, neurodegeneration, Parkinson’s disease, Alzheimer’s disease,
amyotrophic lateral sclerosis, polyglutamine diseases

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Address all correspondence to:
Charleen T. Chu, MD, PhD
Department of Pathology, Division of Neuropathology
University of Pittsburgh School of Medicine
Room W958 BST
200 Lothrop Street
Pittsburgh, PA 15213, USA.
Tel: (412) 383-5379
Fax: (412) 648-9172
E-mail:
ctc4@pitt.edu