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Open AccessJournal ArticleDOI

Protein kinase G confers survival advantage to Mycobacterium tuberculosis during latency-like conditions.

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TLDR
It is proposed that PknG probably acts as a modulator of latency-associated signals, an axis that is dispensable for survival under normoxic conditions but is critical for non-replicating persistence of mycobacteria.
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This article is published in Journal of Biological Chemistry.The article was published on 2017-09-29 and is currently open access. It has received 72 citations till now. The article focuses on the topics: Serine threonine protein kinase & Kinase activity.

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Citations
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The mycobacterial cell envelope — a moving target

TL;DR: The regulatory pathways that control metabolism of the cell wall and surface lipids in M. tuberculosis during growth and stasis are described, and it is speculated about how this regulation might affect antibiotic susceptibility and interactions with the immune system.
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Exosomes in Pathogen Infections: A Bridge to Deliver Molecules and Link Functions.

TL;DR: It is believed that exosomes act as “bridges” during pathogen infections through the mechanisms mentioned above and a balance between infection and anti-infection is hypothesized.
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Tuberculosis and the art of macrophage manipulation

TL;DR: This review focuses on the diverse effectors that Mtb uses in its multipronged effort to subvert the innate immune responses of macrophages, and highlights recent advances in understanding the molecular interface of the Mtb‐macrophage interaction.
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Mycobacterium tuberculosis WhiB3 maintains redox homeostasis and survival in response to reactive oxygen and nitrogen species.

TL;DR: Empirical proof is provided that WhiB3 is required to mitigate redox stress induced by ROS and RNS, which may be important to activate host/bacterial pathways required for the granuloma development and maintenance.
References
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Journal ArticleDOI

Evaluation of a nutrient starvation model of Mycobacterium tuberculosis persistence by gene and protein expression profiling.

TL;DR: A model in which M. tuberculosis arrests growth, decreases its respiration rate and is resistant to isoniazid, rifampicin and metronidazole is established, which is generated a model with which to search for agents active against persistent M.culosis.
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An in vitro model for sequential study of shiftdown of Mycobacterium tuberculosis through two stages of nonreplicating persistence.

TL;DR: It is suggested that the ability to shift down into one or both of the two nonreplicating stages, corresponding to microaerophilic and anaerobic persistence, is responsible for the ability of tubercle bacilli to lie dormant in the host for long periods of time, with the capacity to revive and activate disease at a later time.
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The role of the granuloma in expansion and dissemination of early tuberculous infection.

TL;DR: In this paper, the authors use quantitative intravital microscopy to reveal distinct steps of granuloma formation and assess their consequence for infection, showing that pathogenic mycobacteria exploit the granulomas during the innate immune phase for local expansion and systemic dissemination.
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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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