|
Psoriasis
|
0.420 |
Biomarker
|
disease |
BEFREE |
Taken together this study broadens our understanding about the mechanism of action of PUVA providing possible new strategy targeting proapoptotic function of RIG-1, a regulator of innate immune response or p53 for psoriasis therapy.
|
26518362 |
2016 |
|
Psoriasis
|
0.420 |
Biomarker
|
disease |
BEFREE |
We screened a cDNA library and identified potential RIG-I interacting partners that may play a role in psoriasis.
|
25658361 |
2015 |
|
Psoriasis
|
0.420 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide meta-analysis identifies multiple novel associations and ethnic heterogeneity of psoriasis susceptibility.
|
25903422 |
2015 |
|
Psoriasis
|
0.420 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide comparative analysis of atopic dermatitis and psoriasis gives insight into opposing genetic mechanisms.
|
25574825 |
2015 |
|
Psoriasis
|
0.420 |
Biomarker
|
disease |
CTD_human |
Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity.
|
23143594 |
2012 |
|
Psoriasis
|
0.420 |
GeneticVariation
|
disease |
GWASDB |
Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity.
|
23143594 |
2012 |
|
Psoriasis
|
0.420 |
GeneticVariation
|
disease |
GWASCAT |
Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity.
|
23143594 |
2012 |
|
SINGLETON-MERTEN SYNDROME 2
|
0.410 |
GeneticVariation
|
disease |
BEFREE |
G3BP1 activation of NFATc4 mapped to G3BP1 domains supporting interactions with RIG-I (retinoic acid inducible gene I), a stimulus for mitochondrial antiviral signaling (MAVS) that drives cardiovascular calcification in humans when mutated in Singleton-Merten syndrome (SGMRT2).
|
29626090 |
2018 |
|
SINGLETON-MERTEN SYNDROME 2
|
0.410 |
GeneticVariation
|
disease |
UNIPROT |
Mutations in DDX58, which encodes RIG-I, cause atypical Singleton-Merten syndrome.
|
25620203 |
2015 |
|
SINGLETON-MERTEN SYNDROME 2
|
0.410 |
CausalMutation
|
disease |
CLINVAR |
|
|
|
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Taken together, these data reveal that the NS4A Y16 residue regulates a noncanonical Riplet-TBK1-IRF3-dependent, but RIG-I-MAVS-independent, signaling pathway that limits HCV infection.<b>IMPORTANCE</b> The HCV NS3-NS4A protease complex facilitates viral replication by cleaving and inactivating the antiviral innate immune signaling proteins MAVS and Riplet, which are essential for RIG-I activation.
|
31534039 |
2019 |
|
Hepatitis C
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The current study genotyped two selected SNPs (IFIH1 rs3747517 and DDX58 rs9695310) using TaqMan allelic discrimination assay to assess their association with the susceptibility and clinical outcome of HCV infection among 3065 participants (1545 non-HCV infection individuals, 568 spontaneous HCV clearance cases, and 952 persistent infection patients).
|
30633820 |
2019 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Induction of Selenoprotein P mRNA during Hepatitis C Virus Infection Inhibits RIG-I-Mediated Antiviral Immunity.
|
30974086 |
2019 |
|
Influenza
|
0.400 |
Biomarker
|
disease |
BEFREE |
LEP and DPEP have certain protective effects on the influenza virus-infected mice, which may be associated with their abilities of effectively alleviating lung injury, improving the immunologic function of infected mice and adjusting the host's TLRs and RIG-1 pathways.
|
31551774 |
2019 |
|
Influenza
|
0.400 |
Biomarker
|
disease |
BEFREE |
The rli32-induced IFN-β response is RIG-I (retinoic acid inducible gene I) dependent, and cells primed with rli32 inhibit influenza virus replication.
|
31594810 |
2019 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Although RIG-I has been recognized as the leading cytoplasmic sensor against HCV for a long time, recent findings that MDA5 regulates the IFN response to HCV have emerged.
|
29899107 |
2018 |
|
Influenza
|
0.400 |
Biomarker
|
disease |
BEFREE |
We show here, in the context of an influenza virus infection of lung epithelial cells, that AgNPs down-regulated influenza induced CCL-5 and -IFN-β release (two cytokines important in antiviral immunity) through RIG-I inhibition, while enhancing IL-8 production, a cytokine important for mobilizing host antibacterial responses.
|
29357226 |
2018 |
|
Influenza
|
0.400 |
Biomarker
|
disease |
BEFREE |
RIG-I Signaling via MAVS Is Dispensable for Survival in Lethal Influenza Infection <i>In Vivo</i>.
|
30532653 |
2018 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
RIG-I is an innate immune receptor that detects and responds to infection by deadly RNA viruses such as influenza, and Hepatitis C. In the cytoplasm, RIG-I is faced with a difficult challenge: it must sensitively detect viral RNA while ignoring the abundance of host RNA.
|
28180316 |
2017 |
|
Influenza
|
0.400 |
Biomarker
|
disease |
BEFREE |
RIG-I is an innate immune receptor that detects and responds to infection by deadly RNA viruses such as influenza, and Hepatitis C. In the cytoplasm, RIG-I is faced with a difficult challenge: it must sensitively detect viral RNA while ignoring the abundance of host RNA.
|
28180316 |
2017 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In fact, activation of pathogen sensors induces the expression of CSR32/EGOT RIG-I and the RNA-activated kinase PKR sense HCV RNA, activate NF-κB and upregulate EGOT EGOT is increased in the liver of patients infected with HCV and after infection with influenza or Semliki Forest virus (SFV).
|
27283940 |
2016 |
|
Influenza
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In fact, activation of pathogen sensors induces the expression of CSR32/EGOT RIG-I and the RNA-activated kinase PKR sense HCV RNA, activate NF-κB and upregulate EGOT EGOT is increased in the liver of patients infected with HCV and after infection with influenza or Semliki Forest virus (SFV).
|
27283940 |
2016 |
|
Influenza
|
0.400 |
Biomarker
|
disease |
BEFREE |
Standing on three legs: antiviral activities of RIG-I against influenza viruses.
|
27318973 |
2016 |
|
Hepatitis C
|
0.400 |
Biomarker
|
disease |
BEFREE |
Unexpectedly, the interaction between HCV's 3'UTR and RIG-I seemed to play a minor role in this activation, while another helicase MDA5 played a more important role in sensing HCV infection to trigger interferon response.
|
25463548 |
2015 |
|
Hepatitis C
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Our study reveals an important role of NS5A D2 for suppression of the IFN response that is activated by HCV via RIG-I and MDA5 in a sequential manner.
|
25908268 |
2015 |