Essential role of mda-5 in type I IFN responses to polyriboinosinic:polyribocytidylic acid and encephalomyocarditis picornavirus.

By Leonid Gitlin, W. Barchet, S. Gilfillan, M. Cella, B. Beutler, R. Flavell, Michael S. Diamond, M. Colonna. Proceedings of the National Academy of Sciences of the United States of America, 2006

1,242 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6a9fb26b5c75c0598ffb592f0b786ef547b719f3

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Citations in the corpus

Innate Immunity to Virus Infection (2009, background): “By contrast, MDA5-deficient mice do not respond to infection with picornaviruses, such as encephalomyocarditis virus (EMCV) and Theiler’s virus (15, 17).”
Type I interferons in host defense. (2006, positive): “MDA5 is the primary cytosolic receptor for the RNA polymer poly I:C and is required for detection of the picornavirus encephalomyocarditis virus (EMCV) (Gitlin et al., 2006; Kato et al., 2006).”
TLR3: interferon induction by double-stranded RNA including poly(I:C). (2008, background): “Studies using knock-out mice clearly showed that RIG-I is essential for the production of IFN-α/β in response to RNA viruses whose genomes contain 5′-triphosphate, whereas MDA5 is involved in the detection of picornaviruses [18,19].”
Ribose 2′-O-methylation provides a molecular signature for the distinction of self and non-self mRNA dependent on the RNA sensor Mda5 (2011, neutral): “The replication of encephalomyocarditis virus (family Picornaviridae) seems to be not restricted by IFIT proteins 28 ; however, infection with this virus is sensed through the Mda5 pathway 35 .”
Viral evasion and subversion of pattern-recognition receptor signalling (2008, background): “On the one hand, viruses that produce large amounts of dsRNA during their life cycle, such as picornaviruses, are sensed mainly by MDA5 (Ref”
Recognition of 5′-triphosphate by RIG-I helicase requires short blunt double-stranded RNA as contained in panhandle of negative strand virus (2009, neutral): “, 1992) as well as the two helicases MDA-5 (Gitlin et al., 2006; Kang et al., 2002; Kato et al., 2008; Kato et al., 2006; Takahasi et al., 2008; Yoneyama et al., 2004) and RIG-I (Yoneyama et al.”
Absence of autophagy results in reactive oxygen species-dependent amplification of RLR signaling (2009, background): “This study showed that type I interferons and cytokine production were enhanced in Atg5 / MEFs in response to infection with VSV, which is recognized through RIG-I (15), or to transfection with Poly I:C, which triggers MDA-5-dependent signaling (12, 16).”