Edward A. Burton
University of Pittsburgh
89 Papers
791 Citations
Edward A. Burton is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Zebrafish & Substantia nigra. The author has an hindex of 34, co-authored 83 publications. Previous affiliations of Edward A. Burton include Queen Elizabeth Hospital Birmingham & University of Oxford.
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Papers
Live imaging of mitochondrial dynamics in CNS dopaminergic neurons in vivo demonstrates early reversal of mitochondrial transport following MPP(+) exposure.
April A. Dukes,Qing Bai,Victor S. Van Laar,Yangzhong Zhou,Vladimir Ilin,Christopher N. David,Zeynep Sena Agim,Joshua L. Bonkowsky,Jason R. Cannon,Simon C. Watkins,Claudette M. St. Croix,Edward A. Burton,Sarah B. Berman +12 more
TL;DR: This is the first time mitochondrial transport has been observed directly in CNS dopaminergic neurons of a living vertebrate and quantified in a PD model in vivo, and the findings are compatible with a model in which damage at presynaptic dopamine terminals causes an early compensatory increase in retrograde transport of compromised mitochondria for degradation in the cell body.
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The role of basal and myogenic factors in the transcriptional activation of utrophin promoter A: implications for therapeutic up-regulation in Duchenne muscular dystrophy
TL;DR: This study investigated basal regulation and myogenic induction of promoter A, which provides a basis for further understanding the regulatory mechanisms that control utrophin expression in muscle and may facilitate the development of reagents to effect therapeutic up-regulation of utphin in DMD.
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Replication-defective genomic herpes simplex vectors: design and production.
TL;DR: This work has established sound principles for the straightforward production of large-scale pure preparations of vector stocks for clinical applications and has allowed early steps to be taken towards targeting viral entry to predetermined cellular subsets.
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Delivery using herpes simplex virus: an overview.
William F. Goins,Darren Wolfe,David Krisky,Qing Bai,Edward A. Burton,David J. Fink,Joseph C. Glorioso +6 more
TL;DR: Although the wild-type virus may be reactivated from latency under the influence of a variety of stresses, completely replication defective viruses can be constructed that retain the ability to establish persistent quiescent genomes in neurons, but that are unable to subsequently reactivate in the nervous system.
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α-Synuclein amplifies cytoplasmic peroxide flux and oxidative stress provoked by mitochondrial inhibitors in CNS dopaminergic neurons in vivo
Victor S. Van Laar,Jianming Chen,Alevtina Zharikov,Qing Bai,Roberto Di Maio,April A. Dukes,Teresa G. Hastings,Simon C. Watkins,J. Timothy Greenamyre,Claudette M. St. Croix,Edward A. Burton +10 more
TL;DR: It is shown that motor abnormalities prior to neuronal loss in this model are associated with extensive α-Synuclein-dependent cellular thiol oxidation, and α- Synuclein is a critical determinant of the redox consequences of mitochondrial dysfunction in dopaminergic neurons.
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