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Title: TBK-1 Promotes Autophagy-Mediated Antimicrobial Defense by Controlling Autophagosome Maturation
Authors: Manohar Pilli
John Arko-Mensah
Marisa Ponpuak
Esteban Roberts
Sharon Master
Michael A. Mandell
Nicolas Dupont
Wojciech Ornatowski
Shanya Jiang
Steven B. Bradfute
Jack Ansgar Bruun
Tom Egil Hansen
Terje Johansen
Vojo Deretic
University of New Mexico Health Sciences Center
Mahidol University
Universitetet i Tromso
Keywords: Immunology and Microbiology;Medicine
Issue Date: 24-Aug-2012
Citation: Immunity. Vol.37, No.2 (2012), 223-234
Abstract: Autophagy is a fundamental biological process of the eukaryotic cell contributing to diverse cellular and physiological functions including cell-autonomous defense against intracellular pathogens. Here, we screened the Rab family of membrane trafficking regulators for effects on autophagic elimination of Mycobacterium tuberculosis var. bovis BCG and found that Rab8b and its downstream interacting partner, innate immunity regulator TBK-1, are required for autophagic elimination of mycobacteria in macrophages. TBK-1 was necessary for autophagic maturation. TBK-1 coordinated assembly and function of the autophagic machinery and phosphorylated the autophagic adaptor p62 (sequestosome 1) on Ser-403, a residue essential for its role in autophagic clearance. A key proinflammatory cytokine, IL-1β, induced autophagy leading to autophagic killing of mycobacteria in macrophages, and this IL-1β activity was dependent on TBK-1. Thus, TBK-1 is a key regulator of immunological autophagy and is responsible for the maturation of autophagosomes into lytic bactericidal organelles. © 2012 Elsevier Inc.
ISSN: 10974180
Appears in Collections:Scopus 2011-2015

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