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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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Decreased expression of the vitamin C transporter SVCT1 by ascorbic acid in a human intestinal epithelial cell line.
TL;DR: Results suggest that high-dose supplements might not be the most efficient way of increasing the body pool of vitamin C.
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Elucidating microRNA regulatory networks using transcriptional, post-transcriptional and histone modification measurements
Sara J. C. Gosline,Allan M. Gurtan,Courtney K. JnBaptiste,Andrew D. Bosson,Pamela Milani,Simona Dalin,Bryan J. Matthews,Yoon S. Yap,Phillip A. Sharp,Ernest Fraenkel +9 more
TL;DR: In this article, an approach to characterizing miRNA-regulatory networks by systematically profiling transcriptional, post-transcriptional and epigenetic activity in a pair of isogenic murine fibroblast cell lines with and without Dicer expression is described.
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Dcytb (Cybrd1) functions as both a ferric and a cupric reductase in vitro.
TL;DR: The data suggests that Dcytb plays a physiological role in both iron and copper uptake, through divalent metal transporter 1 (DMT1) and copper transporter 1, respectively, and shows that 59Fe uptake was significantly enhanced in D Cytb‐EGFP expressing MDCK cells which endogenously express DMT1.
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Nanoparticle-mediated delivery of siRNA targeting Parp1 extends survival of mice bearing tumors derived from Brca1-deficient ovarian cancer cells
Michael S. Goldberg,Deyin Xing,Yin Ren,Sandra Orsulic,Sangeeta N. Bhatia,Sangeeta N. Bhatia,Phillip A. Sharp +6 more
TL;DR: The in vivo administration of siRNA to Parp1 in mouse models of ovarian cancer extends the survival of mice bearing tumors derived from Brca1-deficient ovarian cancer cells but not from BrCA1 wild-type cells, confirming the proposed mechanism of synthetic lethality.
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Transcriptional Pause Sites Delineate Stable Nucleosome-Associated Premature Polyadenylation Suppressed by U1 snRNP.
Anthony C. Chiu,Hiroshi I. Suzuki,Xuebing Wu,Dig Bijay Mahat,Andrea J. Kriz,Phillip A. Sharp +5 more
TL;DR: It is reported that U1 snRNP recognition and transcription pausing at stable nucleosomes are linked through premature polyadenylation signal (PAS) termination, and it is proposed that premature PAS termination near the nucleosome-associated pause site represents a common transcriptional elongation checkpoint regulated by U1 snR NP recognition, nucleosom stability, and Myc activity.