anti-DDX58 (DDX58) Antikörper

Human DEAD (Asp-Glu-Ala-Asp) Box Polypeptide 58 (DDX58) Interaktionspartner

1. MiR-545 exerts its effects in pancreatic ductal adenocarcinoma by directly targeting RIG-1

2. 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.

3. critical for the initiation of IRF-3 phosphorylation, dimerization and downstream gene expression during antiviral innate immune response

4. Viral pseudo-enzymes activate RIG-I via deamidation to evade cytokine production.

5. During Crimean-Congo hemorrhagic fever virus infection, RIG-I mediated a type I interferon response via MAVS.

6. TRIM25 plays an additional role in RIG-I/MDA5 signaling other than RIG-I ubiquitination via activation of NF-kappaB.

7. Gal1 and gal3 regulate the inflammatory response in airway epithelial cells exposed to microbial neuraminidase by modulating the expression of SOCS1 and RIG1.

8. 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.

9. our study demonstrates that the novel pathway lncRNA Ftx/miR-545/RIG-I promotes hepatocellular carcinoma development

10. Results provide evidence that RIG-I as an essential mediator for influenza A virus-induced COX-2 expression.

11. this review describes antiviral activities of RIG-I against influenza viruses (standing on three legs)

12. a novel mechanism of pattern recognition receptor modulation by HCV and suggests a biological function of the HCV alternate reading frame in the modulation of host innate immunity

13. Foot-and-mouth disease virus Viroporin 2B antagonizes RIG-I-mediated antiviral effects by inhibition of its protein expression.

14. Study uncovered a novel aspect of Rig-I in monitoring gut microbiota through regulating IgA and IL6-STAT3-dependent Reg3gamma pathway. Besides, Rig-I loss could also promote colorectal cancer progression both in the presence and absence of intestinal bacteria.

15. Data demonstrate that RIG-1 is activated after mitochondrial SUMOylation by MAPL which is an essential process for the mitochondrial antiviral signaling response.

16. The current study establishes that hypoxia can profoundly influence the inducible RIG-I protein expression in malignant cells of both human and murine origin, whereas this phenomenon was not identified in nonmalignant cell lines or primary cells.

17. Oncostatin M induces RIG-I and MDA5 expression and enhances the double-stranded RNA response in fibroblasts.

18. perifascicular pattern of RIG-I expression supports the diagnosis of dermatomyositis

19. Conclusively, these data demonstrate the MCPIP1 contributes to attenuate influenza A virus-induced host antiviral response by suppressing RIG-I expression.

20. Low RIG1 expression is associated with Arenaviral infections.

Mouse (Murine) DEAD (Asp-Glu-Ala-Asp) Box Polypeptide 58 (DDX58) Interaktionspartner

1. RIG-I-mediated antiviral innate immunity requires oxidative phosphorylation activity.

2. MLL5 has a role in suppressing antiviral innate immune response by facilitating STUB1-mediated RIG-I degradation

3. FBXW7 is critical for RIG-I stabilization during antiviral responses.

4. Identification of a second binding site on the RIG-I TRIM25 B30.2 domain has been reported.

5. 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.

6. RNF122 suppresses antiviral type I interferon production by targeting RIG-I caspase activation and recruitment domains to mediate RIG-I degradation.

7. innate immune signaling mediated by RLR plays a critical role in nuclear reprogramming.

8. 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.

9. 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.

10. Collectively, these results uncover an independent functional contribution of the apo-Rig-I/Stat3 interaction in the maintenance of Treg/Th17 cell balance.

11. 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.

12. 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.

13. RIG-I subsequently localized to antiviral stress granules induced after viral replication complexes formation

14. identifies DDX58 and MTHFSD as two TDP-43 targets that are misregulated in amyotrophic lateral sclerosis. 1

15. Data show that preconditioning with poly(I:C) alters toll-like receptors (TLR) and RIG-I-like receptors (RLRs) responses in opposite directions.

16. Cytosolic LMW FGF2 functions as a negative regulator in RIG-I-mediated antiviral signaling.

17. results indicate that Lyn plays a positive regulatory role in RIG-I-mediated interferon expression as a downstream component of IPS-1

18. 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.

19. findings suggest that RIG-I directs a typical IFN-dependent antiviral response against an RNA virus capable of suppressing the RNAi response

20. The results describe a novel, interactive relationship between RIG-I downstream signalling molecules resulting in efficient anti-viral immunity.

Pig (Porcine) DEAD (Asp-Glu-Ala-Asp) Box Polypeptide 58 (DDX58) Interaktionspartner

1. 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.

2. Key regulators involved in Porcine circovirus 2 infection were identified as IFNbeta, DDX58 (RIG-I), and IRF7.

3. 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.

4. Viral RNA polymerase components PB2, PB1, and PA directly target RIG-I.

5. 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.

6. DDX58 had two nonsynonymous SNPs in the helicase domain.