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K. Mark Parnell

Researcher at Yale University

Publications -  6
Citations -  386

K. Mark Parnell is an academic researcher from Yale University. The author has contributed to research in topics: Peptidyl transferase & Ribosome. The author has an hindex of 4, co-authored 6 publications receiving 342 citations.

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Substrate-assisted catalysis of peptide bond formation by the ribosome

TL;DR: Evidence that a functional group on one of the tRNA substrates plays an essential catalytic role in the reaction is reported, suggesting that substrate assistance has been retained as a catalytic strategy during the evolution of the prebiotic peptidyl transferase center into the modern ribosome.
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Mechanism of Inhibition of the Human Immunodeficiency Virus Type 1 Reverse Transcriptase by d4TTP: an Equivalent Incorporation Efficiency Relative to the Natural Substrate dTTP

TL;DR: Using a pre-steady-state kinetic analysis, it is found that d4TTP was incorporated by HIV-1 RT just as efficiently as dTTP during both DNA- and RNA-dependent DNA synthesis.
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Evidence against stabilization of the transition state oxyanion by a pKa-perturbed RNA base in the peptidyl transferase center.

TL;DR: CCdApPmn binds 50S ribosomes with essentially equal affinity at all pH values between 5.0 and 8.5, which argues against a mechanism for peptidyl transfer in which a residue with near neutral pKa stabilizes the transition-state oxyanion, at least to the extent that CCd ApPmn accurately mimics the transition state.
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Monocarboxylate transporter antagonism reveals metabolic vulnerabilities of viral-driven lymphomas.

TL;DR: In this article, the role of MCTs has been studied in EBV-associated malignancies, which display Warburg-like metabolism in vitro, and they showed that EBV infection of B lymphocytes directly promotes temporal induction of monocarboxylate transporters through the viral proteins EBNA2 and LMP1, respectively.
Posted ContentDOI

Monocarboxylate transporter antagonism reveals metabolic vulnerabilities of viral-driven lymphomas

TL;DR: It is shown that EBV infection of B lymphocytes directly promotes temporal induction of MCT1 and MCT4 through the viral proteins EBNA2 and LMP1 respectively, with MCT 1 being induced early after infection and M CT4 late, pointing at a novel therapeutic approach for viral lymphomas.