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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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Growth-dependent expression of dihydrofolate reductase mRNA from modular cDNA genes.

TL;DR: The results suggest that the metabolic state of the cell is important in determining either the efficiency of polyadenylation at various sites or the stability of mRNAPolyadenylated at various Sites in three cell lines.
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Structure of rnas replicated by the dna-dependent t7 rna polymerase

TL;DR: RNAs transcribed from DNA template containing the established sequences of X and Y RNAs were efficiently replicated by T7 RNA polymerase, suggesting that they may resemble tRNA molecules and tRNA-like structures at the 3' termini of many plant viral RNA genomes.
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Structure of late adenovirus 2 heterogeneous nuclear RNA

TL;DR: The structure of steady-state nuclear late adenovirus 2 RNA is consistent with these molecules being intermediates in the intramolecular processing of mRNA from a much longer initial transcript.
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A system for Cre-regulated RNA interference in vivo

TL;DR: Cassettes incorporating various combinations of reporter genes, miRNA-based RNAi (including two shRNA constructs at once), and oncogenes are described and the delivery of effective RNA interference in cells in culture, efficient transduction into hematopoietic stem cells with cell-type-specific knockdown in their progeny, and rapid generation of regulated shRNAs in transgenic mice are demonstrated.
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Conditional Lethal Mutants of Adenovirus 2-Simian Virus 40 Hybrids I. Host Range Mutants of Ad2+ND1

TL;DR: The pattern of protein synthesis in monkey cells is quite different with the mutant resembling Ad2, which is defective in the synthesis of late proteins, however, in human cells, the proteins synthesized by H39 and the parent Ad2(+)ND1 are very similar.