Small self-RNA generated by RNase L amplifies antiviral innate immunity
By K. Malathi, B. Dong, M. Gale, R. Silverman. Nature, 2007
658 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/34ff4545bf4bd7444c9f225212ba2c72fe20c28e
How researchers see this paper
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In Immunology
- Shizuo Akira
- O. Takeuchi
- T. Mogensen
- R. Randall
- Yong‐jun Liu
- Anna Marie Pyle
- S. Goodbourn
- Taro Kawai
In Oncology
- Shizuo Akira
- O. Takeuchi
- T. Mogensen
- M. Gale
- K. Malathi
- Y. Loo
- Praveen Manivannan
- Mohammad Adnan Siddiqui
Citations in the corpus
- Epidemiology of Prostate Cancer (2019, background): “Chromosome 1q24-25 that is referred as HPC1 gene encodes the enzyme ribonuclease L (RNASEL) [56], which is involved in the innate immune defense mechanisms and the interferon (IFN)-mediated signaling [57].”
- ATP hydrolysis by the viral RNA sensor RIG-I prevents unintentional recognition of self-RNA (2015, background): “For instance, RIG-I can bind to endogenous mRNA (Zhang et al., 2013) or RNase-L cleavage products (Malathi et al., 2007), while MDA5 was shown to be activated by mRNA stem loop structures under conditions where reduction of A:T base-paired RNA is not prevented by ADAR1 (Liddicoat et al., 2015).”
- Macrophage activation by endogenous danger signals (2008, background): “In addition to the direct effect by viral RNA, both RIG-I and MDA5 can recognize small self-RNA molecules that are generated by anti-viral endoribonuclease, RNase L [46].”
- Cytosolic Sensing of Viruses (2013, background): “Furthermore, small structured RNaseLcleavage-derived RNAs with a 50 hydroxyl group and a 30 monophosphate were also reported as RIG-I agonists (Malathi et al., 2007).”
- Plasmacytoid dendritic cells: sensing nucleic acids in viral infection and autoimmune diseases (2008, background): “First, a recently described molecule termed DNA-dependent activator of IRFs (DAI) has been shown in vitro to act as a cytosolic DNA sensor by binding dsDNA and signalling through TBK1 and IRF3 to activate NF-κB and induce type I IFN productio”
- Immune signaling by RIG-I-like receptors (2011, background): “Furthermore, RNA cleavage products generated by the 20,50-linked oligoadenylate-activated RNase L ribonuclease can trigger RIG-I- and MDA5-dependent IFN induction, and this may serve as a means to amplify the antiviral response through production of RLR substrates (Malathi et al., 2007, 2010).”
- MDA5/RIG-I and virus recognition. (2008, background): “RNase L, an endonuclease originally thought to cleave viral ssRNA, was reported to be involved in the production of IFN-b in response to RNA virus infection or dsRNA stimulation [19].”
- Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “Intriguingly, the magnitude of IFN induction is enhanced by the activation of RNase L (Malathi et al., 2007), an endonuclease that degrades both cellular and viral RNAs to generate short fragments with 39 monophosphates.”
- RIG-I detects viral genomic RNA during negative-strand RNA virus infection. (2010, background): “Viral genomes, shorter viral transcripts, double-stranded RNA, or cellular RNA cleaved by RNase L have all been suggested to trigger RIG-I (Habjan et al., 2008; Hausmann et al., 2008; Hornung et al., 2006; Kato et al., 2008; Malathi et al., 2007; Pichlmair et al., 2006; Plumet et al., 2007; Ranjith-”
- Structural Basis of RNA Recognition and Activation by Innate Immune Receptor RIG-I (2011, background): “This basic channel may allow RIG-I to recognize dsRNA with 3′ nucleotide overhangs or 3′ monophosphates that are products of RNase L digestio”
- Interferon-inducible antiviral effectors (2008, background): “This accounts for the observation that RNaseL-deficient cells show markedly decreased IFNβ production owing to reduced signalling through these PRR”