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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. dans 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.
Bronchial mucosal IFN-alpha/beta and pattern recognition receptor expression in patients with experimental rhinovirus-induced asthma exacerbations
IFIH1 polymorphisms (rs1990760 and rs3747517) were associated with systemic lupus erythematosus susceptibility and rs1990760 risk T allele related with IL-18 and granzyme B serum levels in SLE patients.
Paramyxovirus V proteins are able to bind to and disrupt the signaling activity of these MDA5 proteins, irrespective of their specific mutations, reducing IFN production and IFN-stimulated gene expression to effectively suppress the hyperactive antiviral response
Analysis of chosen polymorphisms rs2476601 a/G - PTPN22, rs1990760 C/T - IFIH1, rs179247 a/G - TSHR in pathogenesis of autoimmune thyroid diseases in children.
R516Q mutation and their connectivity towards sequence-structural basis dysfunction of MDA5 protein, is reported.
We have identified IRF-1, RIG-I and MDA5 as potent anti-norovirus effectors.
IFIH1 mutation is the cause for the Aicardi goutieres syndrome associated pulmonary hypertension.
Melanoma Differentiation-Associated Gene 5 (MDA5)-mediated activation of interferon beta induction is down-regulated by Hepatitis E Virus (HEV) Papain-Like Cysteine Protease (PCP). MDA5 protein expression is completely abolished in the presence of HEV PCP.
MDA5 forms helical filaments to recognize cytosolic double-stranded RNA. ATP binding and hydrolysis cause structural changes, which are proposed to confer proofreading activity.
Report of three Japanese cases of anti-MDA5 antibody-positive rapidly progressive interstitial lung disease without signs of dermatomyositis. High-resolution computed tomography revealed patchy or subpleural distribution of consolidations and/or ground-glass opacities accompanied by traction bronchiectasis. All patients succumbed to respiratory failure within two months.
This review discusses the evidence for MDA5 activity as a cause of autoimmune disease. [review]
Investigated single-nucleotide polymorphisms (SNPs) in interferon induced with helicase C domain 1 (IFIH1) and their association with genetic predisposition to vitiligo in patients and controls.
Authors found that several 14-3-3 isoforms may interact with MDA5 through the CARDs (N-MDA5), but 14-3-3eta was the only isoform that could enhance MDA5-dependent IFNbeta promoter activities in a dose-dependent manner.
FMDV 2B negatively regulates the retinoic acid inducible gene-I like RNA helicases receptor-mediated IFN-beta induction by targeting RIG-I and MDA5
Low MDA5 expression is associated with severe malaria.
work demonstrates that the increased efficiency of MDA5 in recognizing dsRNA comes at a cost of self-recognition and implicates a unique role of Alu-dsRNAs as virus-like elements that shape the primate immune system.
RIG-I and MDA5 receptor sensing of host non-coding RNAs facilitates the cell-intrinsic immune response to Kaposi's sarcoma-associated herpesvirus infection.
Melanoma differentiation-associated gene 5 (MDA5) is a recently described autoantigen target in a subset of patients with dermatomyositis. Anti-MDA5 dermatomyositis is characterized by a unique mucocutaneous and systemic phenotype
genetic association studies in population of children in Hungary: Data suggest that a genetic polymorphism in IFIH1 (rs1990760) is associated with seasonal variation in onset of type 1 diabetes in population studied; this polymorphism in IFIH1 may contribute to manifestation of type 1 diabetes primarily in summer.
Anti-MDA5 antibody helps in the diagnosis of dermatomyositis, predicting cutaneous, musculoskeletal and pulmonary manifestations.
findings indicate a possible role of PACT in regulating the Cardiovirus-triggered immune responses mediated by MDA5 and LGP2
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 isoform of ADAR1 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-derived reactive oxygen species are necessary for the innate immune response and trigger the induction of RIG-I 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 associated MDA5 in virally-infected cells.
embryonic death and phenotypes of Adar1(E861A/E861A) were rescued by concurrent deletion of the cytosolic sensor of dsRNA, MDA5.
IFIH1 heterozygous mice have a regulatory rather than effector T-cell response at the site of autoimmunity, supporting IFIH1 expression as an essential regulator of the diabetogenic T-cell response.
Our results, therefore, suggest that Arl5B is a negative regulator for MDA5.
TRIM13 interacts with MDA5 and negatively regulates MDA5-mediated type I IFN production
RIG-I and MDA-5 detection of viral RNA-dependent RNA polymerase activity restricts positive-strand RNA virus replication.
MDA5 modulates the development of chronic lung inflammation by regulating the early inflammatory response in the lung.
These results strongly suggest that RIG-I and MDA5 participate in innate antiviral responses in cochlear tissue.
These studies suggest that MDA5 in the immune priming environment shapes optimal CD8(+) T cell activation and subsequent clearance of West Nile virus from the central nervous system.
Thus, RIG-I and MDA5 are essential pattern recognition receptors that recognize distinct pathogen-associated molecular patterns that accumulate during West Nile virus replication.
Collectively, our in vitro and in vivo studies both support a critical role for MDA5 in the innate immune response against hepatitis B virus infection.
study identifies the porcine 2'-5'-oligoadenylate synthetase-like protein (pOASL) as an interferon (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 and MDA5 to initiate the RIG-I 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