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anti-Human DDX58 Antikörper:
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Human Polyclonal DDX58 Primary Antibody für WB - ABIN388602
Bao, Liu, Shan, Li, Garofalo, Casola: Human metapneumovirus glycoprotein G inhibits innate immune responses. in PLoS pathogens 2008
Show all 9 Pubmed References
Human Polyclonal DDX58 Primary Antibody für IHC - ABIN965986
Imaizumi, Aratani, Nakajima, Carlson, Matsumiya, Tanji, Ookawa, Yoshida, Tsuchida, McIntyre, Prescott, Zimmerman, Satoh: Retinoic acid-inducible gene-I is induced in endothelial cells by LPS and regulates expression of COX-2. in Biochemical and biophysical research communications 2002
Show all 8 Pubmed References
Human Polyclonal DDX58 Primary Antibody für IHC - ABIN965987
Cui, Imaizumi, Yoshida, Borden, Satoh: Retinoic acid-inducible gene-I is induced by interferon-gamma and regulates the expression of interferon-gamma stimulated gene 15 in MCF-7 cells. in Biochemistry and cell biology = Biochimie et biologie cellulaire 2004
Show all 6 Pubmed References
Human Polyclonal DDX58 Primary Antibody für IHC - ABIN965985
Yoneyama, Kikuchi, Natsukawa, Shinobu, Imaizumi, Miyagishi, Taira, Akira, Fujita: The RNA helicase RIG-I has an essential function in double-stranded RNA-induced innate antiviral responses. in Nature immunology 2004
Show all 6 Pubmed References
Human Monoclonal DDX58 Primary Antibody für IP, IHC - ABIN1169336
Gack, Nistal-Villán, Inn, García-Sastre, Jung: Phosphorylation-mediated negative regulation of RIG-I antiviral activity. in Journal of virology 2010
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Human Polyclonal DDX58 Primary Antibody für IHC (p), WB - ABIN541284
Alexopoulou, Holt, Medzhitov, Flavell: Recognition of double-stranded RNA and activation of NF-kappaB by Toll-like receptor 3. in Nature 2001
Show all 3 Pubmed References
Human Polyclonal DDX58 Primary Antibody für ELISA - ABIN544642
Li, Chen, Kato, Gale, Lemon: Distinct poly(I-C) and virus-activated signaling pathways leading to interferon-beta production in hepatocytes. in The Journal of biological chemistry 2005
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Human Polyclonal DDX58 Primary Antibody für ELISA - ABIN544644
Breiman, Grandvaux, Lin, Ottone, Akira, Yoneyama, Fujita, Hiscott, Meurs: Inhibition of RIG-I-dependent signaling to the interferon pathway during hepatitis C virus expression and restoration of signaling by IKKepsilon. in Journal of virology 2005
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Human Polyclonal DDX58 Primary Antibody für IHC (p), WB - ABIN2476365
Chapuis, Knobel, Loup, von Niederhäusern: [Isolated renal angiomyolipoma]. in Helvetica chirurgica acta 1976
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Human Polyclonal DDX58 Primary Antibody für EIA, IHC (p) - ABIN5555173
Korolowicz, Iyer, Czerwinski, Suresh, Yang, Padmanabhan, Sheri, Pandey, Skell, Marquis, Kallakury, Tucker, Menne: Antiviral Efficacy and Host Innate Immunity Associated with SB 9200 Treatment in the Woodchuck Model of Chronic Hepatitis B. in PLoS ONE 2017
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these results showed that HSV-1 infection can enhance the expression of RIG-1 in the human term placenta
The authors describe the identification of two heterozygous variants in DExD/H-box helicase 58 (DDX58) encoding the cytosolic RNA receptor RIG-I in a 41-year-old Caucasian male patient with severe influenza virus A infection, suggesting that functional defects in RIG-I increase susceptibility to severe influenza infection in humans.
this study shows that LINE1 contributes to autoimmunity through both RIG-I- and MDA5-mediated RNA sensing pathways
During influenza A virus infection short aberrant RNAs (mini viral RNAs (mvRNAs)), produced by the viral RNA polymerase during the replication of the viral RNA genome, bind to and activate the RNA sensor retinoic acid-inducible gene I (RIG-I) and lead to the expression of interferon-beta.
RIG-I translocates directionally from the dsRNA end into the stem region.
This study suggests that Respiratory syncytial virus NS1 interacts with TRIM25 and interferes with RIG-I ubiquitination to suppress type-I interferon signaling.
The results indicated that RIG-1 (rs3739674 and rs9695310) polymorphisms are associated with an increased risk of enterovirus 71-induced hand, foot, and mouth disease in Chinese children, whereas RIG-1 rs3739674 and TLR3 rs5743305 polymorphisms are associated with disease severity. These findings support an important role of innate immune mechanism in enterovirus 71 infection.
FMDV 2B negatively regulates the retinoic acid inducible gene-I like RNA helicases receptor-mediated IFN-beta induction by targeting RIG-I and MDA5
RIG-I and TLR3 seem to be important factors in the pathogenesis of abdominal aortic aneurysms.
Here, the authors identified multiple RNA regions in Kaposi's sarcoma-associated herpesvirus as potential virus ligands that bind to RIG-I and stimulate RIG-I-dependent but RNA Pol III-independent IFN-beta signaling.
MiR-545 exerts its effects in pancreatic ductal adenocarcinoma by directly targeting RIG-1
miR-34a is an antioncogene in multiple tumors, in this study, RIG-I and miR-34a suppressed cell growth, proliferation, migration, and invasion in cervical cancer cells in vitro. miR-34a was validated as a new regulator of RIG-I by binding to its 3' untranslated region and upregulating its expression level.
critical for the initiation of IRF-3 phosphorylation, dimerization and downstream gene expression during antiviral innate immune response
Viral pseudo-enzymes activate RIG-I via deamidation to evade cytokine production.
During Crimean-Congo hemorrhagic fever virus infection, RIG-I mediated a type I interferon response via MAVS.
TRIM25 plays an additional role in RIG-I/MDA5 signaling other than RIG-I ubiquitination via activation of NF-kappaB.
Gal1 and gal3 regulate the inflammatory response in airway epithelial cells exposed to microbial neuraminidase by modulating the expression of SOCS1 and RIG1.
These observations highlight the importance of RIG-I signaling in anti-HIV innate immunity in macrophages, which may be beneficial for the treatment of HIV and aid in the understanding of the neuropathogenesis of HAND.
our study demonstrates that the novel pathway lncRNA Ftx/miR-545/RIG-I promotes hepatocellular carcinoma development
Results provide evidence that RIG-I as an essential mediator for influenza A virus-induced COX-2 expression.
These findings demonstrate the involvement of RIG-I in the sensing of picornavirus infections and the ability of MDA5 to inhibit viral replication in an IFN-independent manner.
RIG-I-mediated antiviral innate immunity requires oxidative phosphorylation activity.
MLL5 has a role in suppressing antiviral innate immune response by facilitating STUB1-mediated RIG-I degradation
FBXW7 is critical for RIG-I stabilization during antiviral responses.
Identification of a second binding site on the RIG-I TRIM25 B30.2 domain has been reported.
Elevated retinoic acid-inducible gene 1 (RIG-I) modulated the interaction of activated proto-oncogene c-Src (Src) and STAT3 by competitive binding to STAT3.
RNF122 suppresses antiviral type I interferon production by targeting RIG-I caspase activation and recruitment domains to mediate RIG-I degradation.
innate immune signaling mediated by RLR plays a critical role in nuclear reprogramming.
RIG-I expression is markedly increased in the affected skin derived from psoriasis patients and from both IL-23- and imiquimod -induced psoriasis-like mouse model.
Toll-like receptor 2 (TLR2) and retinoic acid-inducible gene I (RIG-I) cooperatively initiate innate immune responses to MuV infection in mouse ovarian granulosa cells.
Collectively, these results uncover an independent functional contribution of the apo-Rig-I/Stat3 interaction in the maintenance of Treg/Th17 cell balance.
The RIG-I, as well as the adaptor protein mitochondrial antiviral signaling protein, regulates NF-kappaB-mediated induction of adhesion molecules and proinflammatory cytokine expression in response to LPS.
Data suggest that activation of either RIG-I/MAVS or STING pathways during acute intestinal tissue injury in mice resulted in IFN-I signaling that maintained gut 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 targets that are misregulated in amyotrophic lateral sclerosis. 1
Data show that preconditioning with poly(I:C) alters toll-like receptors (TLR) and RIG-I-like receptors (RLRs) responses in opposite directions.
Cytosolic LMW FGF2 functions as a negative regulator in RIG-I-mediated antiviral signaling.
results indicate that Lyn plays a positive regulatory role in RIG-I-mediated interferon expression as a downstream component of IPS-1
In lung epithelial cells, retinoic acid-inducible gene-1 (RIG-I) was identified as the major RIG-I-like receptor required for RSV-induced protease expression via MAVS.
findings suggest that RIG-I directs a typical IFN-dependent antiviral response against an RNA virus capable of suppressing the RNAi response
These results indicate for the first time that TRIM25 inhibits Porcine reproductive and respiratory virus replication and that the N protein antagonizes the antiviral activity by interfering with TRIM25-mediated RIG-I ubiquitination.
This study indicated that RIG-I showed an antiviral role against Seneca valley virus and was essential for activation of type I IFN signaling during SVV infection.
Key regulators involved in Porcine circovirus 2 infection were identified as IFNbeta, DDX58 (RIG-I), and IRF7.
RIG-I and TLR3 interact with the pseudoknot of Porcine Reproductive and Respiratory Syndrome Virus 3' untranslated regions. Both RIG-I and TLR3 are required for the pseudoknot to induce interferon 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 to initiate the RIG-I signaling pathway to trigger innate defenses against infection.
DDX58 had two nonsynonymous SNPs in the helicase 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