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David R. Sherman

Researcher at University of Washington

Publications -  119
Citations -  14423

David R. Sherman is an academic researcher from University of Washington. The author has contributed to research in topics: Mycobacterium tuberculosis & Tuberculosis. The author has an hindex of 51, co-authored 114 publications receiving 12964 citations. Previous affiliations of David R. Sherman include Seattle Biomed & Center for Infectious Disease Research and Policy.

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A small-molecule nitroimidazopyran drug candidate for the treatment of tuberculosis.

TL;DR: It is concluded that nitroimidazopyrans offer the practical qualities of a small molecule with the potential for the treatment of tuberculosis and bactericidal activity against both replicating and static M. tuberculosis.
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Inhibition of Respiration by Nitric Oxide Induces a Mycobacterium tuberculosis Dormancy Program

TL;DR: It is shown that O2 and low, nontoxic concentrations of NO competitively modulate the expression of a 48-gene regulon, which is expressed in vivo and prepares bacilli for survival during long periods of in vitro dormancy, and leads to a model postulating that, within granulomas, inhibition of respiration by NO production and O2 limitation constrains M. tuberculosis replication rates in persons with latent tuberculosis.
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Regulation of the Mycobacterium tuberculosis hypoxic response gene encoding α-crystallin

TL;DR: The results suggest a possible role for Rv3132c/3133c/Rv3134c in mycobacterial latency, and an apparent operon that includes the putative two-component response regulator pair R v3133/3132/3134/3 134c is suggested.
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Rv3133c/dosR is a transcription factor that mediates the hypoxic response of Mycobacterium tuberculosis.

TL;DR: Results demonstrate that Rv3133c/DosR is a transcription factor of the two‐component response regulator class, and that it is the primary mediator of a hypoxic signal within M. tuberculosis.
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Deletion of RD1 from Mycobacterium tuberculosis Mimics Bacille Calmette-Guérin Attenuation

TL;DR: It was concluded that genes within or controlled by RD1 are essential for MTB virulence and that loss of RD1 was important in BCG attenuation.