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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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Effect of the tripartite leader on synthesis of a non-viral protein in an adenovirus 5 recombinant

TL;DR: It is demonstrated that coinfection of 293 cells with this recombinant and wild type Adenovirus 5 also results in decreased EIb mRNA synthesis, and proposed that the overproduction of polypeptide IX suppresses mRNA expression from the EIB and IX promoter sites, probably by an autoregulation loop active during lytic growth.
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Function and localization of microRNAs in mammalian cells.

TL;DR: Various mechanisms by which miRNAs regulate posttranscriptional level-mediating translational repression and/or mRNA degradation-through their association with Argonaute protein and target mRNAs are discussed, including their subcellular localization.
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Ctr1 and its role in body copper homeostasis.

TL;DR: This data indicates that Ctr1-transfected cell lines exhibit saturable, pH-dependent Cu(I) uptake indicating a role in copper transport, and suggests an essential function in mammalian embryonic development since homozygous mutants die in utero.
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Establishment of mammalian cell lines containing multiple nonsense mutations and functional suppressor tRNA genes

TL;DR: The generation of mammalian cell lines carrying functional amber suppressor genes is described, which are stable and exhibit normal growth rates.
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Promoter-specific hypoacetylation of X-inactivated genes

TL;DR: The histone H4 acetylation status of the active X (Xa) and inactive X (Xi) chromosomes was investigated at the level of individual genes and it was found that promoters of X-inactivated genes were markedly hypoacetylated, which coincided with the methylation of adjacent CG dinucleotides.