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Vojo Deretic

Researcher at University of New Mexico

Publications -  278
Citations -  51981

Vojo Deretic is an academic researcher from University of New Mexico. The author has contributed to research in topics: Autophagy & Phagosome. The author has an hindex of 101, co-authored 269 publications receiving 45639 citations. Previous affiliations of Vojo Deretic include University of Texas at Austin & University of Michigan.

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Therapeutic targeting of autophagy in neurodegenerative and infectious diseases

TL;DR: Rubinsztein, Bento, and Deretic discuss the beneficial roles of autophagy in the context of infectious and neurodegenerative diseases.
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Rab14 is critical for maintenance of Mycobacterium tuberculosis phagosome maturation arrest.

TL;DR: A critical role for the small GTPase Rab14 is demonstrated in maintaining mycobacterial phagosome maturation block and enables myc Cobacterium tuberculosis phagosomes to maintain early endosomal characteristics and avoid late endOSomal/lysosomal degradative components.
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Functional equivalence of Escherichia coli sigma E and Pseudomonas aeruginosa AlgU: E. coli rpoE restores mucoidy and reduces sensitivity to reactive oxygen intermediates in algU mutants of P. aeruginosa.

TL;DR: It is reported that E. coli sigma E can complement phenotypic defects of algU inactivation in P. aeruginosa and it is suggested that elements showing sequence similarity to those known to regulate AlgU activity in MucA are also present in other bacteria.
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Galectins Control mTOR in Response to Endomembrane Damage

TL;DR: It is shown that mTOR is inhibited by lysosomal damage, and a novel galectin-based signal-transduction system, termed here GALTOR, intersects with the known regulators of mTOR on theLysosome and controls them in response to lysOSomal damage.
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Analysis of the oxyR-ahpC region in isoniazid-resistant and -susceptible Mycobacterium tuberculosis complex organisms recovered from diseased humans and animals in diverse localities.

TL;DR: The data are consistent with the hypothesis that some polymorphisms located in the ahpC-oxyR intergenic region are selected for after reduction in catalase or peroxidase activity attributable to katG alterations arising with INH therapy.