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This study evaluation the roles of SOCS1 (show SOCS1 ELISA Kits), the regulator of TLR9 (show TLR9 ELISA Kits), RIG-I, and CD152 (show CTLA4 ELISA Kits) in patients with liver fibrosis/cirrhosis; the use of polymorphisms as markers for genetic risk is reported.
study documents that recombinant measles virus produce defective interfering genomes that have high immunostimulatory properties via their binding to RIG-I and LGP2 (show DHX58 ELISA Kits) proteins, both of which are cytosolic nonself RNA sensors of innate immunity.
findings define the WHIP (show WRNIP1 ELISA Kits)-TRIM14 (show TRIM14 ELISA Kits)-PPP6C (show PPP6C ELISA Kits) mitochondrial signalosome required for RIG-I-mediated innate antiviral immunity.
both IL-6 (show IL6 ELISA Kits) and RIG-I are downstream molecules of STING along the DNA sensor pathway.
These data suggest that prior exposure to IFN-gamma (show IFNG ELISA Kits) may leave an epigenetic mark on the chromatin that enhances airway cells' ability to resist infection, possibly via epigenetic upregulation of RIG-I.
findings show that RIG-I and MDA5 (show IFIH1 ELISA Kits) triggering by dengue virus leads to TH1 (show TH1L ELISA Kits) polarization, which is characterized by high levels of IFN-gamma (show IFNG ELISA Kits); identified RIG-I and MDA5 (show IFIH1 ELISA Kits) as critical players in innate and adaptive immune responses against Dengue virus
Results identified a negative-feedback mechanism that targets RIG-I activity mediated by DAPK1 (show DAPK1 ELISA Kits). RIG-I-mediated antiviral signaling activates DAPK1 (show DAPK1 ELISA Kits) kinase activity and DAPK1 (show DAPK1 ELISA Kits) inactivates RIG-I RNA sensing by direct phosphorylation of RIG-I.
Mechanistically, West Nile virus NS1 (show PTPN11 ELISA Kits) targets RIG-I and melanoma differentiation-associated gene 5 (MDA5 (show IFIH1 ELISA Kits)) by interacting with them and subsequently causing their degradation by the proteasome.
RIG-I stimulates the cellular innate immunity against hepatitis E virus infections.
dynamic sumoylation and desumoylation of MDA5 (show IFIH1 ELISA Kits) and RIG-I modulate efficient innate immunity to RNA virus and its timely termination.
Collectively, these results uncover an independent functional contribution of the apo (show C9orf3 ELISA Kits)-Rig-I/Stat3 (show STAT3 ELISA Kits) interaction in the maintenance of Treg/Th17 cell balance.
The RIG-I, as well as the adaptor protein mitochondrial antiviral signaling protein (show MAVS ELISA Kits), regulates NF-kappaB (show NFKB1 ELISA Kits)-mediated induction of adhesion molecules and proinflammatory cytokine expression in response to LPS (show TLR4 ELISA Kits).
Data suggest that activation of either RIG-I/MAVS (show MAVS ELISA Kits) or STING pathways during acute intestinal tissue injury in mice resulted in IFN-I signaling that maintained gut (show GUSB ELISA Kits) epithelial barrier integrity and reduced GVHD severity.
RIG-I subsequently localized to antiviral stress granules induced after viral replication complexes formation
identifies DDX58 and MTHFSD as two TDP-43 (show TARDBP ELISA Kits) targets that are misregulated in amyotrophic lateral sclerosis. 1
Data show that preconditioning with poly(I:C) alters toll (show TLR4 ELISA Kits)-like receptors (TLR) and RIG-I-like receptors (RLRs) responses in opposite directions.
Cytosolic LMW FGF2 (show FGF2 ELISA Kits) functions as a negative regulator in RIG-I-mediated antiviral signaling.
results indicate that Lyn (show LYN ELISA Kits) plays a positive regulatory role in RIG-I-mediated interferon (show IFNA ELISA Kits) expression as a downstream component of IPS-1 (show ISYNA1 ELISA Kits)
In lung epithelial cells, retinoic acid-inducible gene-1 (show RARRES3 ELISA Kits) (RIG-I) was identified as the major RIG-I-like receptor required for RSV-induced protease expression via MAVS (show MAVS ELISA Kits).
findings suggest that RIG-I directs a typical IFN-dependent antiviral response against an RNA virus capable of suppressing the RNAi response
Viral RNA polymerase components PB2, PB1, and PA directly target RIG-I.
These data indicate that classical swine fever virus can be recognized by both RIG-I and MDA5 (show IFIH1 ELISA Kits) to initiate the RIG-I signaling pathway to trigger innate defenses against infection.
DDX58 had two nonsynonymous SNPs in the helicase (show DNA2 ELISA Kits) domain.
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.
DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide RIG-I
, probable ATP-dependent RNA helicase DDX58
, putative ATP-dependent RNA helicase DDX58
, retinoic acid-inducible protein I
, DEAD (Asp-Glu-Ala-Asp) box polypeptide 58
, probable ATP-dependent RNA helicase DDX58-like
, DEAD box protein 58
, DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide
, RIG-I-like receptor 1
, RNA helicase RIG-I
, retinoic acid inducible gene I
, retinoic acid-inducible gene 1 protein
, retinoic acid-inducible gene I protein
, DEAD-box protein 58
, DEAD/H box polypeptide RIG-I
, retinoic acid-inducible gene-I
, RNA helicase induced by virus