NLRX1 is a regulator of mitochondrial antiviral immunity
Chris B. Moore,
Daniel T. Bergstralh,
Joseph A. Duncan,
Yu Lei,
Thomas E. Morrison,
Albert G. Zimmermann,
Mary A. Accavitti-Loper,
Victoria J. Madden,
Lijun Sun,
Zhengmao Ye,
John D. Lich,
Mark T. Heise,
Zhijian Chen and
Jenny P-Y. Ting ()
Additional contact information
Chris B. Moore: Department of Microbiology-Immunology,
Daniel T. Bergstralh: Lineberger Comprehensive Cancer Center,
Joseph A. Duncan: Department of Medicine, Division of Infectious Diseases
Yu Lei: Department of Microbiology-Immunology,
Thomas E. Morrison: Department of Genetics,
Albert G. Zimmermann: Department of Microbiology-Immunology,
Mary A. Accavitti-Loper: University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
Victoria J. Madden: University of North Carolina, Chapel Hill, North Carolina 27599, USA
Lijun Sun: Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
Zhengmao Ye: Department of Microbiology-Immunology,
John D. Lich: Department of Microbiology-Immunology,
Mark T. Heise: Department of Genetics,
Zhijian Chen: Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
Jenny P-Y. Ting: Department of Microbiology-Immunology,
Nature, 2008, vol. 451, issue 7178, 573-577
Abstract:
Cytoplasmic RIG-like helicases are sensors of viral RNA, and signal through the mitochondrial adaptor protein MAVS to activate IRF3 and induce type 1 interferon production. This paper shows that a member of the NLR family of proteins called NLRX1 is a negative regulator of the pathway and functions by inhibiting the interaction of the viral sensor with the MAVS adaptor.
Date: 2008
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:451:y:2008:i:7178:d:10.1038_nature06501
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DOI: 10.1038/nature06501
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