The RNA Helicase Lgp2 Inhibits TLR-Independent Sensing of Viral Replication by Retinoic Acid-Inducible Gene-I1

By S. Rothenfusser, Nadège Goutagny, Gary DiPerna, Mei-jiao Gong, Brian G. Monks, A. Schoenemeyer, Masahiro Yamamoto, Shizuo Akira, Katherine A. Fitzgerald. Journal of Immunology, 2005

671 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/ad00586a5f11079865f341fb322d5b349367d43a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Shizuo Akira
2. O. Takeuchi
3. Satoshi Uematsu
4. T. Mogensen
5. R. Medzhitov
6. Taro Kawai
7. Mitsutoshi Yoneyama
8. T. Fujita

In Oncology

1. Shizuo Akira
2. O. Takeuchi
3. Satoshi Uematsu
4. T. Mogensen
5. R. Randall
6. S. Goodbourn
7. Taro Kawai
8. R. Medzhitov

Citations in the corpus

• Toll-like receptors and innate immunity (2006, background): “Like RIG-I, overexpression of MDA5 enhanced NDV-induced type I IFN production and antiviral responses in response to VSV or EMCV.”
• Double-Stranded RNA Is Produced by Positive-Strand RNA Viruses and DNA Viruses but Not in Detectable Amounts by Negative-Strand RNA Viruses (2006, background): “On the other hand, however, the dsRNA-binding proteins MDA-5 (which is inhibited by paramyxoviruses) (4) and RIG-I both are important sensor molecules for negative-strand RNA viruses (45, 48, 71).”
• The interferon response circuit: Induction and suppression by pathogenic viruses (2005, background): “A third member of the RIG-I helicase family, LGP2, is a natural inhibitor which presumably masks the viral dsRNA from recognition by RIG-I or MDA5 and serves as a negative regulator of IFN gene expression (Rothenfusser et al., 2005; Yoneyama et al., 2005).”
• Pathogen recognition and innate immunity. (2006, positive): “The protein LGP2 also shares homology with RIG-I in the helicase domain, although it lacks a CARD (Rothenfusser et al., 2005; Yoneyama et al., 2005).”
• Innate Immunity to Virus Infection (2009, background): “Initially, both RIG-I and MDA5 were implicated in the recognition of polyI:C, a synthetic analogue of viral dsRNA (6, 9, 10).”
• Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “induce signaling but rather prevents RIG-I signaling (310),”
• Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “…activators of RIG-I and mda-5 remain uncertain (see below), RIG-I was identified initially as an essential regulator for poly(rI).poly(rC)-induced signalling in a functional screen (Yoneyama et al., 2004) and binds to poly(rI).poly(rC) in vitro (Rothenfusser et al., 2005; Yoneyama et al., 2005).”
• Systems biology approach predicts immunogenicity of the yellow fever vaccine in humans (2008, neutral): “13).”
• 5′-triphosphate RNA requires base-paired structures to activate antiviral signaling via RIG-I (2009, methodology): “(3); 24 h after transfection, the cells were stimulated with the indicated RNA oligonucleotides for 12 h.”