LGP2 is a positive regulator of RIG-I– and MDA5-mediated antiviral responses
By T. Satoh, H. Kato, Y. Kumagai, Mitsutoshi Yoneyama, Shintaro Sato, Kazufumi Matsushita, T. Tsujimura, T. Fujita, Shizuo Akira, O. Takeuchi. Proceedings of the National Academy of Sciences of the United States of America, 2010
663 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/455627147e25a586d4d0958df3cfa42443465cab
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Citations in the corpus
- Signaling in innate immunity and inflammation. (2012, background): “RIG-I recognizes double-stranded RNAs (dsRNAs) that have a 5′ triphosphate and are either viral in origin or Table 3.”
- Pathogen Recognition by the Innate Immune System (2011, background): “viral infection, suggesting that the ATPase activity of RLR members may be essential for antiviral responses [46].”
- The Airway Epithelium: Soldier in the Fight against Respiratory Viruses (2011, background): “Recently, a new member of the RIG-I-like RNA helicase family, namely, LGP2, has been suggested to play an important role in picornavirus recognition by facilitating viral RNA recognition by RIG-I and MDA5 through its ATPase domain (255).”
- Netting Neutrophils Are Major Inducers of Type I IFN Production in Pediatric Systemic Lupus Erythematosus (2011, background): “IFN-a up-regulates the transcription of RNA receptors including not only TLR7 but also LGP2, a member of the cytoplasmic DExD/H box–containing RNA helicase family that mediates RNA conformational changes promoting recognition by RIG-I and MDA5 and downstream signaling (39).”
- Mitochondria in innate immune responses (2011, background): “Although LGP2 was initially suggested to function as a negative regulator of RIG-I and MDA5 signalling, a more recent study indicates that LGP2 positively regulates RIG-I- and MDA5-dependent antiviral response”
- ATP hydrolysis by the viral RNA sensor RIG-I prevents unintentional recognition of self-RNA (2015, background): “LGP2 has augmenting and regulatory roles in MDA5 and RIG-I dependent signaling (Bruns et al., 2014; Satoh et al., 2010; Sparrer and Gack, 2015).”
- Immune signaling by RIG-I-like receptors (2011, background): “…negative regulation of RLR signaling (Bamming and Horvath, 2009; Li et al., 2009b), cells that express an LGP2 mutant that has lost its ATP hydrolyzing activity are similarly impaired in signaling of IFN induction in response to RNA virus infection as are cells lacking LGP2 (Satoh et al., 2010).”
- A structure-based model of RIG-I activation. (2012, background): “The function of LGP2 is less clearly defined, because it can act positively or negatively upon activation by different viruses (Saito et al. 2007; Satoh et al. 2010).”
- Pattern recognition receptors and inflammation. (2010, background): “However, the generation of LGP2 À/À mice and mice with a point mutation, D30A, that disrupts the ATPase activity of LGP2 revealed that LGP2 positively regulates production of type I IFNs in response to RNA viruses recognized by both RIG-I and MDA5 (Satoh et al., 2010).”
- Structural insights into RNA recognition by RIG-I (2011, neutral): “The function of LGP-2 is less clearly defined, as it can act positively or negatively upon activation by different viruses (Saito et al., 2007; Satoh et al., 2010).”