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Human IFIH1 Protein expressed in HEK-293 Cells - ABIN2722584
Labrador-Horrillo, Martinez, Selva-OCallaghan, Trallero-Araguas, Balada, Vilardell-Tarres, Juárez: Anti-MDA5 antibodies in a large Mediterranean population of adults with dermatomyositis. in Journal of immunology research 2014
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These findings indicate that human parainfluenza virus type 2 V binding to MDA5 is important for HPIV-2 virulence in nonhuman primates and that some V protein residues involved in MDA5 binding are not essential for efficient HPIV-2 growth in vitro.
data highlight new function of ARRDC4 in innate immunity, contributing to the better understanding about regulation of MDA5 activation after EV71 infection, and also suggest ARRDC4 may serve as a potential target for intervention of EV71-induced inflammatory response.
Both diseases (Neuroinflammation and the Singleton-Merten Syndrome) are part of the interferonopathy grouping and that the Arg822Gln mutation in IFIH1 can cause a spectrum of disease, including neurological involvement.
Knockdown of PBRM1 (show PBRM1 Proteins) in colon cancer cells increased the expression of two receptor genes (RIG-I (show DDX58 Proteins) and MDA5) and upregulated interferon (show IFNA Proteins) (IFN)-related and inflammation-related gene signatures.
Dengue virus infection of human dendritic cells drives follicular T helper cells formation via crosstalk of RIG-I (show DDX58 Proteins) and MDA5.
study revealed that encapsidation of DI-RNA (defective interfering genomes) molecules within the measles virus nucleocapsid abolished their immunoactive properties. identified specific interactions of DI-RNAs with both RIG-I (show DDX58 Proteins) and LGP2 (show DHX58 Proteins) but not MDA5.
An up-regulation of type I IFN-induced gene transcripts in all 5 patients tested and a heterozygous gain-of-function mutation in IFIH1 in each family were discovered in families with a Singleton-Merten syndrome phenotype.
Data indicate autosomal recessive, homozygous MDA5 encoding gene IFIH1 mutation in the proband, and both parents and a brother were carriers of this mutation.
this study shows that PACT (show RBBP6 Proteins) facilitates RNA-induced formation of MDA5 oligomers in response to viruses
Human peripheral blood mononuclear cells (PBMCs) and cell lines expressing the risk variant IFIH1(T946) exhibited heightened basal and ligand-triggered production of type I interferons.
Mechanistically, West Nile virus NS1 (show PTPN11 Proteins) targets RIG-I (show DDX58 Proteins) and melanoma differentiation-associated gene 5 (MDA5) by interacting with them and subsequently causing their degradation by the proteasome.
findings indicate a possible role of PACT (show RBBP6 Proteins) in regulating the Cardiovirus-triggered immune responses mediated by MDA5 and LGP2 (show DHX58 Proteins)
These findings imply that MDA5-induced cell death and inflammation in the pancreas facilitate progression to autoimmune destruction of pancreatic beta-cells.
Mice with a knock-in mutation encoding IFIH1(T946) displayed enhanced basal expression of type I interferons, survived a lethal viral challenge and exhibited increased penetrance in autoimmune models, including a combinatorial effect with other risk variants. Furthermore, IFIH1(T946) mice manifested an embryonic survival defect consistent with enhanced responsiveness to RNA self ligands.
TRIM65 as an essential component for the MDA5 signaling pathway and provide physiological evidence showing that ubiquitination is important for MDA5 oligomerization and activation.
MDA-5 stimulation leads to endothelial dysfunction.
The p150 (show ABL1 Proteins) isoform of ADAR1 (show ADAR Proteins) uniquely regulated the MDA5 pathway.
MDA5, detects viral RNA and triggers induction of type I interferons, chemical messengers that induce inflammation and help regulate the immune responses.
Duox2 (show DUOX1 Proteins)-derived reactive oxygen species are necessary for the innate immune response and trigger the induction of RIG-I (show DDX58 Proteins) and MDA5 to resist influenza A infection in human nasal epithelium and mouse nasal mucosa.
L region antisense RNA of EMCV is a key determinant of innate immunity to the virus and represents an RNA that activates LGP2 (show DHX58 Proteins) associated MDA5 in virally-infected cells.
embryonic death and phenotypes of Adar1 (show ADAR Proteins)(E861A/E861A) were rescued by concurrent deletion of the cytosolic sensor of dsRNA, MDA5.
study identifies the porcine 2'-5'-oligoadenylate synthetase-like protein (pOASL) as an interferon (show IFNA Proteins) (IFN)-stimulated gene (ISG) against classical swine fever virus (CSFV); show that pOASL, as an MDA5-interacting protein, is a coactivator of MDA5-mediated IFN induction to exert anti-CSFV actions
These data indicate that classical swine fever virus can be recognized by both RIG-I (show DDX58 Proteins) and MDA5 to initiate the RIG-I (show DDX58 Proteins) signaling pathway to trigger innate defenses against infection.
crystal structure of the MDA5 ATP-hydrolysis domain in complex with parainfluenzavirus 5 V protein; the V protein unfolded the ATP-hydrolysis domain of MDA5 and recognized a structural motif of MDA5 normally buried in the helicase fold leading to disruption of MDA5 ATP-hydrolysis site and prevention of RNA-bound MDA5 filament formation
IFIH1 had only one nonsynonymous SNP in the helicase domain.
DEAD box proteins, characterized by the conserved motif Asp-Glu-Ala-Asp (DEAD), are putative RNA helicases. They are implicated in a number of cellular processes involving alteration of RNA secondary structure such as translation initiation, nuclear and mitochondrial splicing, and ribosome and spliceosome assembly. Based on their distribution patterns, some members of this family are believed to be involved in embryogenesis, spermatogenesis, and cellular growth and division. This gene encodes a DEAD box protein that is upregulated in response to treatment with beta-interferon and a protein kinase C-activating compound, mezerein. Irreversible reprogramming of melanomas can be achieved by treatment with both these agents\; treatment with either agent alone only achieves reversible differentiation. Genetic variation in this gene is associated with diabetes mellitus insulin-dependent type 19.
interferon-induced helicase C domain-containing protein 1
, melanoma differentiation associated protein-5
, melanoma differentiation-associated protein 5
, CADM-140 autoantigen
, DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide
, RIG-I-like receptor 2
, RNA helicase-DEAD box protein 116
, clinically amyopathic dermatomyositis autoantigen 140 kDa
, helicase with 2 CARD domains
, murabutide down-regulated protein
, interferon induced with helicase C domain protein 1
, melanoma differentiation associated protein 5