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Cytoplasmic Listeria monocytogenes stimulates IFN‐β synthesis without requiring the adapter protein MAVS
Author(s) -
Soulat Didier,
Bauch Angela,
Stockinger Silvia,
Superti-Furga Giulio,
Decker Thomas
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.03.057
Subject(s) - irf3 , signal transducing adaptor protein , listeria monocytogenes , cytoplasm , biology , interferon , rna , transfection , virology , rna interference , gene silencing , gene , rna silencing , microbiology and biotechnology , bacteria , biochemistry , genetics , transcription factor
The mitochondria‐associated adapter protein MAVS (also called IPS‐1, VISA or CARDIF, designated MAVS for reasons of simplicity in our manuscript) relays signals from cytoplasmic sensors of viral RNA to the IRF3 kinase complex and the interferon‐β (IFN‐β) gene. Using siRNA‐mediated knock‐down in macrophages we show that IFN‐β synthesis in response to transfected, intracellular double‐stranded RNA (dsRNA), a pathogen‐associated molecular pattern of viruses, is decreased in absence of MAVS. By contrast, the Gram‐positive bacterium Listeria monocytogenes targets the IFN‐β gene without detectable MAVS requirement. The data show that MAVS is not a central adapter protein for all cytoplasmic pathogen sensors that stimulate IFN‐β synthesis.