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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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Assembly of adenovirus major capsid protein is mediated by a nonvirion protein

TL;DR: The assembly of hexon, the major capsid protein of adenovirus, was investigated with the use of conformation-specific monoclonal antibodies to reveal the unique nature of this structure, which is a trimer of three identical monomers folded into a highly conserved and stable structure.
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Purification of the cellular C1 factor required for the stable recognition of the Oct-1 homeodomain by the herpes simplex virus alpha-trans-induction factor (VP16).

TL;DR: The biochemical purification of the mammalian C1 factor suggests that it is composed of multiple subunits of related, but heterogeneous, polypeptides, suggesting that this factor may be a critical target for the regulation of the herpes simplex virus alpha/IE transcription.

Argonaute-Bound Small RNAs from Promoter-Proximal RNA Polymerase II

TL;DR: In this article, a mouse embryonic stem cell system was adapted to express a single epitope-tagged Ago protein family member in an inducible manner, and the authors reported the small RNA profile of Ago-deficient cells and showed that Ago-dependent stability is a common feature of mammalian miRNAs.
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Ubiquitination of RNA polymerase II large subunit signaled by phosphorylation of carboxyl-terminal domain

TL;DR: A sensitive assay using biotinylated ubiquitin revealed extensive ubiquitination of the large subunit of RNA polymerase II during incubations of transcription reactions in vitro.
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A Latent Pro-Survival Function for the Mir-290-295 Cluster in Mouse Embryonic Stem Cells

TL;DR: The pro-survival phenotype shown here may be most relevant to stressful gestations, where pro-oxidant metabolic states induce DNA damage, and may mediate chemotherapeutic resistance in a neoplastic context, making it a useful clinical target.