D
Don W. Cleveland
Researcher at University of California, San Diego
Publications - 453
Citations - 91939
Don W. Cleveland is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Amyotrophic lateral sclerosis & SOD1. The author has an hindex of 152, co-authored 444 publications receiving 84737 citations. Previous affiliations of Don W. Cleveland include Emory University & Johns Hopkins University.
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Peptide mapping by limited proteolysis in sodium dodecyl sulfate and analysis by gel electrophoresis.
TL;DR: A rapid and convenient method for peptide mapping of proteins has been developed that involves partial enzymatic proteolysis in the presence of sodium dodecyl sulfate and analysis of the cleavage products by polyacrylamide gel electrophoresis.
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Number and evolutionary conservation of α- and β-tubulin and cytoplasmic β- and γ-actin genes using specific cloned cDNA probes
Don W. Cleveland,Margaret A. Lopata,Raymond J. MacDonald,Nicholas J. Cowan,William J. Rutter,Marc W. Kirschner +5 more
TL;DR: Bacterial clones containing inserted DNA sequences specific for α- Tubulin, β-tubulin,β-Actin and γ-actin have been constructed from mRNA of embryonic chick brain and are able to hybridize under stringent conditions to DNA of all vertebrates tested, as well as to sea urchin DNA, but not to yeast DNA.
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Onset and Progression in Inherited ALS Determined by Motor Neurons and Microglia
Séverine Boillée,Koji Yamanaka,Christian S. Lobsiger,Neal G. Copeland,Nancy A. Jenkins,George Kassiotis,George Kollias,Don W. Cleveland +7 more
TL;DR: Onset and progression of amyotrophic lateral sclerosis represent distinct disease phases defined by mutant action within different cell types to generate non–cell-autonomous killing of motor neurons; these findings validate therapies, including cell replacement, targeted to the non-neuronal cells.
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An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria
Philip C. Wong,Carlos A. Pardo,David R. Borchelt,Michael K. Lee,Neal G. Copeland,Nancy A. Jenkins,Sangram S. Sisodia,Don W. Cleveland,Don W. Cleveland,Donald L. Price +9 more
TL;DR: Mutations in Cu/Zn superoxide dismutase cause a subset of cases of familial amyotrophic lateral sclerosis, and four lines of mice accumulating one of these mutant proteins (G37R) develop severe, progressive motor neuron disease.
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Decoding ALS: from genes to mechanism
TL;DR: Extraordinary progress in understanding the biology of ALS provides new reasons for optimism that meaningful therapies will be identified, and emerging themes include dysfunction in RNA metabolism and protein homeostasis, with specific defects in nucleocytoplasmic trafficking.