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Robert Child

Researcher at National Institutes of Health

Publications -  14
Citations -  1093

Robert Child is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Francisella tularensis & Francisella. The author has an hindex of 14, co-authored 14 publications receiving 995 citations. Previous affiliations of Robert Child include Rocky Mountain Laboratories & Utah State University.

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Selective Subversion of Autophagy Complexes Facilitates Completion of the Brucella Intracellular Cycle

TL;DR: It is shown that Brucella replication in the ER is followed by BCV conversion into a compartment with autophagic features (aBCV), demonstrating that Bru Cella selectively co-opts autophagy-initiation complexes to subvert host clearance and promote infection.
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Intracellular biology and virulence determinants of Francisella tularensis revealed by transcriptional profiling inside macrophages.

TL;DR: Deletion of FTT0383, F TT0369c or FTT1676 abolished the ability of Schu S4 to survive or proliferate intracellularly and cause lethality in mice, therefore identifying novel determinants of Francisella virulence from their intrACEllular expression profile.
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Brucella Modulates Secretory Trafficking via Multiple Type IV Secretion Effector Proteins

TL;DR: It is demonstrated that Brucella modulates secretory trafficking via multiple T4SS effector proteins that likely act coordinately to promote BrucellA pathogenesis.
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Sensing of Bacterial Type IV Secretion via the Unfolded Protein Response

TL;DR: It is shown that translocation of the T4SS substrate VceC into host cells induces proinflammatory responses, which results in the induction of proinflammatory host cell responses during B. abortus infection.
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Cytosolic clearance of replication-deficient mutants reveals Francisella tularensis interactions with the autophagic pathway

TL;DR: It is demonstrated that replication-impaired strains of Francisella are cleared by autophagy, while replication-competent bacteria seem to interfere with autophagic recognition, therefore ensuring survival and proliferation.