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David S. Bredt
Researcher at Johnson & Johnson
Publications - 224
Citations - 63974
David S. Bredt is an academic researcher from Johnson & Johnson. The author has contributed to research in topics: Nitric oxide synthase & Nitric oxide. The author has an hindex of 107, co-authored 223 publications receiving 62332 citations. Previous affiliations of David S. Bredt include Johns Hopkins University & Georgetown University Medical Center.
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Journal ArticleDOI
Actinin-associated LIM protein-deficient mice maintain normal development and structure of skeletal muscle.
TL;DR: In this paper, the authors describe the generation and analysis of mice lacking the actinin-associated LIM protein (ALP) gene and show that the absence of a dystrophic phenotype in these mice suggests that down-regulation of ALP does not participate in facioscapulohumeral muscular dystrophy.
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Distribution of postsynaptic density proteins in rat kidney: relationship to neuronal nitric oxide synthase.
Akihiro Tojo,David S. Bredt,David S. Bredt,David S. Bredt,Christopher S. Wilcox,Christopher S. Wilcox,Christopher S. Wilcox +6 more
TL;DR: PSD-93 is the predominant PSD expressed in the rat kidney and is located primarily in the basolateral membranes of distal nephron and colocalizes with a pool of nNOS in cytoplasmic vesicles and basol lateral membranes of macula densa cells.
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Early events in glutamate receptor trafficking
Wim Vandenberghe,David S. Bredt +1 more
TL;DR: This work shows that receptor exit from the endoplasmic reticulum represents a critical regulatory step in glutamate receptor trafficking to the neuronal cell surface.
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Identification of a monogenic locus (jams1) causing juvenile audiogenic seizures in mice.
Hidemi Misawa,Elliott H. Sherr,David J. Lee,Dane M. Chetkovich,Andrew Y. Y. Tan,Christoph E. Schreiner,David S. Bredt +6 more
TL;DR: It is reported that Black Swiss mice have a heretofore unrecognized specific susceptibility to audiogenic seizures, which may provide important insight into the fundamental mechanisms for developmentally regulated human epilepsy syndromes.
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Polyamine regulation of ion channel assembly and implications for nicotinic acetylcholine receptor pharmacology.
TL;DR: It is revealed that cellular polyamines control nicotinic acetylcholine receptor (nAChR) biogenesis, and either catabolic degradation or inhibition of polyamine production augments nACh R assembly.