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Beverly L. Davidson

Researcher at Children's Hospital of Philadelphia

Publications -  410
Citations -  35019

Beverly L. Davidson is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: Gene silencing & RNA interference. The author has an hindex of 94, co-authored 391 publications receiving 33041 citations. Previous affiliations of Beverly L. Davidson include United States Department of Veterans Affairs & University of California, Los Angeles.

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Optimization of feline immunodeficiency virus vectors for RNA interference.

TL;DR: The hypothesis that vectors based on feline immunodeficiency virus (FIV) could be used for coexpression of reporter constructs and RNAi expression cassettes was tested and suggested that steric factors, including RNA structure and recruitment of competing transcriptional machinery, may affect gene expression from FIV vectors.
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Human hypoxanthine-guanine phosphoribosyltransferase: a single nucleotide substitution in cDNA clones isolated from a patient with Lesch-Nyhan syndrome (HPRTMidland)

TL;DR: The molecular basis for hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency in a patient, J.H., with Lesch-Nyhan syndrome is determined and a variant of HPRT is designated HPRTMidland.
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Apical barriers to airway epithelial cell gene transfer with amphotropic retroviral vectors.

TL;DR: It is demonstrated that sialic acid, keratan sulfate and collagen type V are present on the apical surface of well-differentiated human airway epithelia and enzyme treatment reduced the abundance of these components, but also decreased the transepithelial resistance to ~35% of the controls, suggesting that the epithelial integrity was impaired.
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In vivo delivery of DN:REST improves transcriptional changes of REST-regulated genes in HD mice.

TL;DR: It is shown that delivery of DN:REST in the motor cortex restores brain-derived neurotrophic factor mRNA and protein levels by reducing endogenous REST occupancy at the Bdnf locus and suggests that a more widespread rescue of REST-regulated sites in the affected brain regions may be necessary.
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Intracellular Trafficking of the JNCL Protein CLN3

TL;DR: It is confirmed by immunohistochemistry and brefeldin A treatment that NH2-terminal green fluorescence protein (GFP)-CLN3 fusion proteins were retained in the Golgi apparatus, with no colocalization with mitochondrial markers, confirming that CLN3 traffics through the ER and Golgi.