Differential roles of MDA5 and RIG-I helicases in the recognition of RNA viruses

By H. Kato, O. Takeuchi, Shintaro Sato, Mitsutoshi Yoneyama, Masahiro Yamamoto, Kosuke Matsui, Satoshi Uematsu, A. Jung, Taro Kawai, K. Ishii and 8 more. Nature, 2006

4,033 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/cd4d0ca7ffa3e4eb65a8d5eddc0119dd64e3fc95

How researchers see this paper

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

In Immunology

In Molecular Biology

Citations in the corpus

Preference of RIG-I for short viral RNA molecules in infected cells revealed by next-generation sequencing (2010, background): “Some viruses, such as picornaviruses and influenza virus, appear to be recognized by only one of the sensors, with picornaviruses being sensed by MDA5 and influenza viruses by RIG-I (1, 8, 9).”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “Thus, in addition to TLRs, cytosolic PRRs with the ability to sense intracellular PAMPs also seem to be important for both immediate innate protection and bridging to the adaptive immune response (93, 174, 372).”
The perfect mix: recent progress in adjuvant research (2007, background): “RIG-I responds to RNA viruses, including paramyxoviruses, influenza virus and Japanese encephalitis virus, whereas MDA5 detects picornaviruse”
NF-κB and the immune response (2006, background): “Recently, it was shown that RIG-I and MDA5 differentially recognize various groups of RNA viruses and are thus critical for a robust antiviral response (Kato et al., 2006).”
Type I interferon inhibits interleukin-1 production and inflammasome activation. (2011, background): “…the DExD/H box RNA helicase family, which serve as the primary intracellular sensors for viral RNA and subsequently initiate signaling cascades leading to type I interferon (IFN) production, thereby establishing an antiviral state (Kato et al., 2006; Nakhaei et al., 2009a; Yoneyama et al., 2004).”
Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes (2020, neutral): “Irf1–/– (Matsuyama et al., 1993), Stat1–/– (Durbin et al., 1996), Ripk3–/– (Newton et al., 2004), Ripk3–/–Fadd–/– (Dillon et al., 2012), Ripk3–/–Casp8–/– (Oberst et al., 2011), Apaf1–/– (JAX, #004373) (Honarpour et al., 2000), Nos2–/– (JAX, #002609) (Laubach et al., 1995), Casp7–/– (Lakhani 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).”
The specific and essential role of MAVS in antiviral innate immune responses. (2006, background): “A recent study has shown that poly(I:C) induces interferons through Mda5, but not RIG-I (Kato et al., 2006).”
Type 1 diabetes: etiology, immunology, and therapeutic strategies. (2011, neutral): “cytoplasmic sensor for viral infection (221, 291).”
Influenza A Virus Panhandle Structure Is Directly Involved in RIG-I Activation and Interferon Induction (2015, background): “The indispensable role of RIG-I in IFN response to IAV infection has long been observed (1, 51); however, the nature of the RIG-I ligands from IAV is not well understood.”