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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.


RIG-I, retinoic acid-inducible gene I
DEAD box proteins, characterized by the conserved motif Asp-Glu-Ala-Asp (DEAD), are putative RNA helicases which are implicated in a number of cellular processes involving RNA binding and alteration of RNA secondary structure. This gene encodes a protein containing RNA helicase-DEAD box protein motifs and a caspase recruitment domain (CARD). It is involved in viral double-stranded (ds) RNA recognition and the regulation of immune response. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, MDA5, VISA, CAN, Interferon Regulatory Factor-3
Papers using RIG-I antibodies
Kinetic analysis of epidermal growth factor receptor somatic mutant proteins shows increased sensitivity to the epidermal growth factor receptor tyrosine kinase inhibitor, erlotinib.
Sherry Barbara, In PLoS Pathogens, 2005
... MARCH5, TANK, GIDE, TRAF6, TRAF3, NEMO, MAVS and RIG-I cDNAs were amplified by PCR from thymus cDNA library (Clontech) and subsequently cloned into ...
Papers on RIG-I
Swift and Strong NK Cell Responses Protect 129 Mice against High-Dose Influenza Virus Infection.
Fang et al., Beijing, China. In J Immunol, Feb 2016
In addition, we identified that early activation of TLRs and RIG-I signaling in 129 mice resulted in quick production of type 1 IFNs and inflammatory cytokines, which are important reasons for the swift kinetics of NK cell responses post influenza virus infection.
Beyond the Inflammasome: Regulatory NLR Modulation of the Host Immune Response Following Virus Exposure.
Allen et al., Moldova. In J Gen Virol, Feb 2016
These NLRs uniquely function to modulate signaling pathways initiated by other families of pattern recognition receptors, such as Toll-like Receptors (TLRs) and/or Rig-I-like Helicase Receptors (RLRs).
Regulation of antiviral innate immune signaling by stress-induced RNA granules.
Onomoto et al., Chiba, Japan. In J Biochem, Feb 2016
Retinoic acid inducible gene I (RIG-I)-like receptors (RLRs) detect viral non-self RNA in cytoplasm of virus-infected cells and play a critical role in the clearance of the invaded viruses through production of antiviral cytokines.
Links between recognition and degradation of cytoplasmic viral RNA in innate immune response.
Daito et al., Sapporo, Japan. In Rev Med Virol, Jan 2016
Cytoplasmic viral RNA is recognized by retinoic acid-inducible gene I (RIG-I)-like receptors, which trigger type I interferon (IFN) production.
The Roles of RNase-L in Antimicrobial Immunity and the Cytoskeleton-Associated Innate Response.
Hassel et al., Baltimore, United States. In Int J Mol Sci, Dec 2015
The active nuclease then cleaves ssRNAs, both cellular and viral, leading to downregulation of their expression and the generation of small RNAs capable of activating retinoic acid-inducible gene-I (RIG-I)-like receptors or the nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome.
RIG-I-like receptors and autoimmune diseases.
Fujita et al., Kyoto, Japan. In Curr Opin Immunol, Dec 2015
RIG-I-like receptors (RLRs) are viral RNA sensors and are essential for type I IFN induction.
Innate Immunity Evasion by Enteroviruses: Insights into Virus-Host Interaction.
Wang et al., Beijing, China. In Viruses, Dec 2015
EVs, which are positive-sense single-stranded RNA viruses, trigger activation of the host antiviral innate immune responses through pathogen recognition receptors such as retinoic acid-inducible gene (RIG-I)-likeand Toll-like receptors.
Poly(I:C) increases the expression of mPGES-1 and COX-2 in rat primary microglia.
Fiebich et al., Belo Horizonte, Brazil. In J Neuroinflammation, Dec 2015
Polyinosinic-polycytidylic acid [poly(I:C)] is a synthetic analog of dsRNA that activates different molecules, such as retinoic acid-inducible gene I, melanoma differentiation-associated gene 5, and toll-like receptor-3 (TLR3).
Mumps virus-induced innate immune responses in mouse Sertoli and Leydig cells.
Han et al., Beijing, China. In Sci Rep, Dec 2015
This study showed that MuV induced innate immune responses in mouse Sertoli and Leydig cells through TLR2 and retinoic acid-inducible gene I (RIG-I) signaling, which result in the production of proinflammatory cytokines and chemokines, including TNF-α, IL-6, MCP-1, CXCL10, and type 1 interferons (IFN-α and IFN-β).
Deubiquitinase MYSM1 Regulates Innate Immunity through Inactivation of TRAF3 and TRAF6 Complexes.
Gekara et al., Umeå, Sweden. In Immunity, Nov 2015
Pattern-recognition receptors (PRRs) including Toll-like receptors, RIG-I-like receptors, and cytoplasmic DNA receptors are essential for protection against pathogens but require tight control to avert inflammatory diseases.
Dengue subgenomic RNA binds TRIM25 to inhibit interferon expression for epidemiological fitness.
Ooi et al., Singapore, Singapore. In Science, Nov 2015
PR-2B sfRNA showed sequence-dependent binding to and prevention of tripartite motif 25 (TRIM25) deubiquitylation, which is critical for sustained and amplified retinoic acid-inducible gene 1 (RIG-I)-induced type I interferon expression.
A Conserved Histidine in the RNA Sensor RIG-I Controls Immune Tolerance to N1-2'O-Methylated Self RNA.
Schlee et al., Bonn, Germany. In Immunity, Aug 2015
The cytosolic helicase retinoic acid-inducible gene-I (RIG-I) initiates immune responses to most RNA viruses by detecting viral 5'-triphosphorylated RNA (pppRNA).
A Sense of Self: RIG-I's Tolerance to Host RNA.
Schoggins, Dallas, United States. In Immunity, Aug 2015
The innate immune sensor RIG-I recognizes viral RNA while avoiding unwanted activation by self RNA.
Reciprocal cellular cross-talk within the tumor microenvironment promotes oncolytic virus activity.
Bell et al., Ottawa, Canada. In Nat Med, May 2015
In turn, CAFs produced high levels of fibroblast growth factor 2 (FGF2), initiating a signaling cascade in cancer cells that reduced retinoic acid-inducible gene I (RIG-I) expression and impeded the ability of malignant cells to detect and respond to virus.
An Overview of Pathogen Recognition Receptors for Innate Immunity in Dental Pulp.
Park et al., Seoul, South Korea. In Mediators Inflamm, 2014
Currently identified PRR families are the Toll-like receptors (TLRs), the C-type lectin receptors (CLRs), the nucleotide-binding oligomerization domain-like receptors (NLRs), the retinoic acid-inducible gene-I-like receptors (RLRs), and the AIM2-like receptor (ALR).
Identification of multiple RIG-I-specific pathogen associated molecular patterns within the West Nile virus genome and antigenome.
Fredericksen et al., College Park, United States. In Virology, 2012
These results suggested that West Nile virus evades the host response by sequestering RIG-I-specific pathogen associated molecular patterns within the complete genome and antigenome at early times post-infection.
Ubiquitin-induced oligomerization of the RNA sensors RIG-I and MDA5 activates antiviral innate immune response.
Chen et al., Dallas, United States. In Immunity, 2012
Mutations of conserved residues in RIG-I that disrupt ubiquitin binding also abrogate its IRF3 activation. Polyubiquitin binding induced a large complex consisting of 4 RIG-I & 4 ubiquitin chains which activated the antiviral signaling cascades.
The mitochondrial targeting chaperone 14-3-3ε regulates a RIG-I translocon that mediates membrane association and innate antiviral immunity.
Gale et al., Seattle, United States. In Cell Host Microbe, 2012
14-3-3epsilon is essential for the stable interaction of RIG-I with TRIM25, which facilitates RIG-I ubiquitination and initiation of innate immunity against hepatitis C virus and other pathogenic RNA viruses.
Expression of the class II tumor suppressor gene RIG1 is directly regulated by p53 tumor suppressor in cancer cell lines.
Chang et al., Taipei, Taiwan. In Febs Lett, 2012
RIG1 gene is a downstream target of p53 in cancer cell lines
Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner.
Paessler et al., Galveston, United States. In Plos Negl Trop Dis, 2011
These studies also demonstrated for the first time that RIG-I was required for interferon-beta production during Junin virus infection.
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