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Phillip A. Sharp

Researcher at Massachusetts Institute of Technology

Publications -  618
Citations -  125567

Phillip A. Sharp is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: RNA & Gene. The author has an hindex of 172, co-authored 614 publications receiving 117126 citations. Previous affiliations of Phillip A. Sharp include McGovern Institute for Brain Research & Medical Research Council.

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Inhibition of transcription factor activity by poliovirus

TL;DR: Results indicate that at least one factor required for specific transcription by polymerase II is deficient in extracts from poliovirus-infected cells.
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Analysis of chlorogenic acids in beverages prepared from Chinese health foods and investigation, in vitro, of effects on glucose absorption in cultured Caco-2 cells

TL;DR: Analysis of the (poly)phenols in these aqueous extracts suggested that dicaffeoylquinic acids and flavanols may be particularly important in producing these effects, suggesting that this merits evaluation in a clinical study.
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Transcription of Simian virus 40 DNA in a HeLa whole cell extract.

TL;DR: The whole cell extract of HeLa cells containing RNA polymerase II and other factors recognize specific sites on linear simian virus 40 (SV40) DNA for initiation of transcription, probably initiating transcription on linear SV40 DNA in vitro at the same sites as RNAs synthesized in vivo.
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Inhibition of adenovirus early region IV transcription in vitro by a purified viral DNA binding protein

TL;DR: It is reported here that the primary product of the EII region, a 72,000 molecular weight DNA-binding protein3 (DBP), specifically represses transcription from the EIV promoter in an in vitro transcription system.

Endogenous miRNA and Target Concentrations Determine Susceptibility to Potential ceRNA Competition

TL;DR: In this paper, the authors characterize and quantitatively quantitate miRNA networks in two cell types, i.e., single-cell reporters and single-antenna cells, and estimate that ∼3,000 additional high-affinity target sites can affect active miRNA families with low endogenous miRNA:target ratios.