Stephen J. Plotch
Memorial Sloan Kettering Cancer Center
17 Papers
290 Citations
Stephen J. Plotch is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: RNA & Transcription (biology). The author has an hindex of 12, co-authored 17 publications.
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Papers
Both the 7-methyl and the 2'-O-methyl groups in the cap of mRNA strongly influence its ability to act as primer for influenza virus RNA transcription
TL;DR: The results indicate that the cap 1 structure found in all mammalian cellular mRNAs is more stringently required for priming influenza virus RNA transcription than for translation in cell-free systems.
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Influenza virion transcriptase: synthesis in vitro of large, polyadenylic acid-containing complementary RNA.
Stephen J. Plotch,R M Krug +1 more
TL;DR: The influenza virion transcriptase is capable of synthesizing in vitro complementary RNA (cRNA) that is similar in several characteristics to the cRNA synthesized in the infected cell, which is the viral mRNA.
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Segments of Influenza Virus Complementary RNA Synthesized In Vitro
Stephen J. Plotch,Robert M. Krug +1 more
TL;DR: In the presence of Mg(2+) and a specific primer, ApG or GpG, the influenza WSN virion transcriptase synthesizes large, polyadenylic acid-containing complementary RNA (cRNA) and results suggest that the in vitro cRNA segments are shorter than, and thus incomplete transcripts of the corresponding vRNA segments.
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Identification of the RNA region transferred from a representative primer, β-globin mRNA, to influenza mRNA during in vitro transcription
TL;DR: 125I-labeled oligonucleotides recovered from the viral mRNA in minor yields indicated that shorter 5' terminal pieces of beta-globin mRNA were sometimes transferred and that G was probably the first base inserted by transcription.
In vitro splicing of influenza viral NS1 mRNA and NS1-beta-globin chimeras: possible mechanisms for the control of viral mRNA splicing.
Stephen J. Plotch,Robert M. Krug +1 more
TL;DR: Two mechanisms are proposed whereby NS1 mRNA splicing in infected cells is controlled via the accessibility of its 3' splice site, which is structurally inaccessible to components of the splicing machinery.
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