D
David W. Martin
Researcher at University of Toronto
Publications - 184
Citations - 12127
David W. Martin is an academic researcher from University of Toronto. The author has contributed to research in topics: Purine nucleoside phosphorylase & Purine metabolism. The author has an hindex of 56, co-authored 177 publications receiving 11791 citations. Previous affiliations of David W. Martin include Technion – Israel Institute of Technology & Laboratory of Molecular Biology.
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Functional recovery in parkinsonian monkeys treated with GDNF.
Don M. Gash,Zhiming Zhang,Aliza Ovadia,Wayne A. Cass,Ai Yi,Linda A. Simmerman,D Russell,David W. Martin,Paul A. Lapchak,Frank H. Collins,B J Hoffer,Greg A. Gerhardt +11 more
TL;DR: Evaluating the effects of GDNF injected intracerebrally into rhesus monkeys that have had the symptomatology and pathophysiological features of Parkinson's disease induced by the neurotoxin 1-methyl-4-phenyl-l,2,3,6-tetrahydropyridine indicates that GDNF may be of benefit in the treatment of Parkinson’s disease.
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Changes in plasma HIV-1 RNA and CD4+ lymphocyte counts and the risk of progression to AIDS. Veterans Affairs Cooperative Study Group on AIDS.
William A. O'Brien,Pamela M. Hartigan,David W. Martin,James Esinhart,Andrew Hill,Sharon L. Benoit,Marc Rubin,Michael S. Simberkoff,John D. Hamilton +8 more
TL;DR: Treatment-induced changes in the plasma HIV-1 RNA level and the CD4+ lymphocyte count are valid predictors of the clinical progression of HIV-related disease and can be used to assess the efficacy of zidovudine and possibly other antiretroviral drugs as well.
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Tau consists of a set of proteins with repeated C-terminal microtubule-binding domains and variable N-terminal domains.
TL;DR: Portions of tau proteins generated by in vitro translation were used to show that these repeats represent tubulin-binding domains, two of which are sufficient to bind to microtubules assembled from purified tubulin in the presence of taxol.
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Control of Specific Gene Expression in Higher Organisms
Gordon M. Tomkins,Thomas D. Gelehrter,Daryl K. Granner,David W. Martin,Herbert H. Samuels,E. Brad Thompson +5 more
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Defects in nuclear structure and function promote dilated cardiomyopathy in lamin A/C–deficient mice
Vesna Nikolova,Christiana Leimena,Aisling C. McMahon,Ju-Chiat Tan,Suchitra Chandar,Dilesh Jogia,Scott H. Kesteven,Jan Michalicek,Robyn Otway,Fons Verheyen,S. Rainer,Colin L. Stewart,David W. Martin,Michael P. Feneley,Diane Fatkin +14 more
TL;DR: It is suggested that lamin A/C-deficient mice develop rapidly progressive dilated cardiomyopathy (DCM), a model in which the primary pathophysiological mechanism in Lmna(-/-) mice is defective force transmission resulting from disruption of lamin interactions with the muscle-specific desmin network and loss of cytoskeletal tension.