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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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A nuclear factor that binds to a conserved sequence motif in transcriptional control elements of immunoglobulin genes.
TL;DR: It is reported here the identification of a human B-cell nuclear factor (IgNF-A) that binds to DNA sequences in the upstream regions of both the mouse heavy and κ light-chain gene promoters and also to the mouseHeavychain gene enhancer.
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Divergent Transcription from Active Promoters
Amy C. Seila,J. Mauro Calabrese,Stuart S. Levine,Gene W. Yeo,Peter B. Rahl,Ryan A. Flynn,Richard A. Young,Phillip A. Sharp +7 more
TL;DR: Evidence of widespread divergent transcription at protein-encoding gene promoters is presented and it is suggested that Divergent transcription over short distances is common for active promoters and may help promoter regions maintain a state poised for subsequent regulation.
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Genome editing with Cas9 in adult mice corrects a disease mutation and phenotype
Hao Yin,Wen Xue,Sidi Chen,Roman L. Bogorad,Eric Benedetti,Markus Grompe,Victor Koteliansky,Phillip A. Sharp,Tyler Jacks,Daniel G. Anderson +9 more
TL;DR: In this article, the authors demonstrate CRISPR-Cas9-mediated correction of a Fah mutation in hepatocytes in a mouse model of the human disease hereditary tyrosinemia.
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Suppression of non-small cell lung tumor development by the let-7 microRNA family
Madhu S. Kumar,Stefan J. Erkeland,Ryan E. Pester,Cindy Y. Chen,Margaret S. Ebert,Phillip A. Sharp,Tyler Jacks +6 more
TL;DR: It is shown that let-7 functionally inhibits non-small cell tumor development and was more potent in lung cancer cell lines harboring oncogenic K-Ras mutations than in lines with other mutations.