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Paul A. Hyslop
Researcher at Eli Lilly and Company
Publications - 63
Citations - 7837
Paul A. Hyslop is an academic researcher from Eli Lilly and Company. The author has contributed to research in topics: DNA damage & NAD+ kinase. The author has an hindex of 32, co-authored 61 publications receiving 7659 citations. Previous affiliations of Paul A. Hyslop include Scripps Health & Scripps Research Institute.
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Journal ArticleDOI
Functional gamma-secretase inhibitors reduce beta-amyloid peptide levels in brain
H. F. Dovey,V. John,J. P. Anderson,L. Z. Chen,P. De Saint Andrieu,L. Y. Fang,S. B. Freedman,B. Folmer,E. Goldbach,E. J. Holsztynska,K. L. Hu,K. L. Johnson-Wood,S. L. Kennedy,D. Kholodenko,J. E. Knops,L. H. Latimer,Michael K. Lee,Z. Liao,I. M. Lieberburg,R. N. Motter,L. C. Mutter,J. Nietz,K. P. Quinn,K. L. Sacchi,P. A. Seubert,G. M. Shopp,E. D. Thorsett,J. S. Tung,J. Wu,S. Yang,C. T. Yin,D. B. Schenk,Patrick C. May,L. D. Altstiel,M. H. Bender,Leonard N. Boggs,T. C. Britton,J. C. Clemens,D. L. Czilli,D. K. Dieckman-Mcginty,J. J. Droste,Kimberly S. Fuson,Bruce D. Gitter,Paul A. Hyslop,E. M. Johnstone,W.-Y. Li,Sheila P. Little,T. E. Mabry,F. D. Miller,Binhui Ni,J. S. Nissen,Warren J. Porter,B. D. Potts,Jon K. Reel,D. Stephenson,Y. Su,L. A. Shipley,C. A. Whitesitt,T. Yin,James E. Audia +59 more
TL;DR: These studies represent the first demonstration of a reduction of brain Aβin vivo and will enable a clinical examination of the Aβ hypothesis that Aβ peptide drives the neuropathology observed in Alzheimer's disease.
Journal ArticleDOI
Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition.
Kelly R. Bales,Tatyana Verina,Richard C. Dodel,Richard C. Dodel,Yansheng Du,Larry Altstiel,Mark H. Bender,Paul A. Hyslop,Edward M. Johnstone,Sheila P. Little,David J. Cummins,Pedro Piccardo,Bernardino Ghetti,Steven M. Paul +13 more
Journal ArticleDOI
Mechanisms of oxidant-mediated cell injury. The glycolytic and mitochondrial pathways of ADP phosphorylation are major intracellular targets inactivated by hydrogen peroxide.
Paul A. Hyslop,D B Hinshaw,W A Halsey,Ingrid U. Schraufstatter,R D Sauerheber,Roger G. Spragg,J H Jackson,Charles G. Cochrane +7 more
TL;DR: Both the estimated rates of ADP phosphorylation by glycolysis and mitochondria and the estimated rate of ATP hydrolysis by ongoing metabolism were utilized to model the approximate decline in intracellular ATP expected at 15-min exposure to various H2O2 concentrations.
Journal ArticleDOI
Oxidant injury of cells. DNA strand-breaks activate polyadenosine diphosphate-ribose polymerase and lead to depletion of nicotinamide adenine dinucleotide.
TL;DR: Results suggest that DNA damage induced within seconds after addition of oxidant may lead to stimulation of poly-ADP-ribose polymerase, and a consequent fall in NAD sufficient to interfere with ATP synthesis.
Journal ArticleDOI
Hydrogen peroxide-induced injury of cells and its prevention by inhibitors of poly(ADP-ribose) polymerase
Ingrid U. Schraufstatter,Paul A. Hyslop,D B Hinshaw,Roger G. Spragg,Larry A. Sklar,Charles G. Cochrane +5 more
TL;DR: In the current studies, inhibition of poly(ADP-ribose) polymerase by 3-aminobenzamide, nicotinamide, or theophylline in cells exposed to lethal concentrations of H2O2 prevented the sequence of events that eventually led to cell lysis--i.e., the decrease in NAD, followed by depletion of ATP, influx of extracellular Ca2+, actin polymerization and, finally, cell death.