RNA- and Virus-Independent Inhibition of Antiviral Signaling by RNA Helicase LGP2

MDA5 RNA Helicase A RNA Silencing Sendai virus RIG-I IRF3 Transcription
DOI: 10.1128/jvi.01325-06 Publication Date: 2006-11-27T23:43:39Z
ABSTRACT
ABSTRACT Antiviral innate immune responses can be triggered by accumulation of intracellular nucleic acids resulting from virus infections. Double-stranded RNA (dsRNA) detected the cytoplasmic helicase proteins RIG-I and MDA5, two that share sequence similarities within a caspase recruitment domain (CARD) DExD/H box domain. These are considered dsRNA sensors thought to transmit signal mitochondrial adapter, IPS-1 (also known as MAVS, VISA, or CARDIF) via CARD interactions. coordinates activity protein kinases activate transcription factors needed induce beta interferon (IFN-β) gene transcription. Another protein, LGP2, lacks region does not IFN-β expression. LGP2 mRNA is induced interferon, treatments, Sendai infection acts feedback inhibitor for antiviral signaling. Results indicate inhibit signaling independently intermediates engaging in complex with IPS-1. Experiments suggest compete kinase IKKi IKKε) common interaction site on results provide first demonstration an element negative-feedback regulation LGP2.
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