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

1. HPV E6 oncoprotein antagonizes the activation of the cytoplasmic innate immune sensor RIG-I by targeting its upstream regulatory enzymes TRIM25 (show TRIM25 Proteins) and USP15 (show USP15 Proteins). We further show that the RIG-I signaling cascade is important for an antiviral innate immune response to HPV16 infection

2. The host RIG-I signaling pathway is a key early obstacle to paramyxovirus infection, as it results in rapid induction of an antiviral response. This study shows that paramyxovirus V proteins interact with and inhibit the activation of RIG-I, thereby interrupting the antiviral signaling pathway and facilitating virus replication.

3. These findings indicated that hepatitis B virus-induced miR146a attenuates cell-intrinsic anti-viral innate immunity through targeting RIG-I and RIG-G.

4. Taken together, these findings reveal an essential role of CypA (show PPIA Proteins) in boosting RIG-I-mediated antiviral immune responses by controlling the ubiquitination of RIG-I and MAVS (show MAVS Proteins).

5. RIG-I-like receptors (RLRs) are well-known viral RNA sensors in the cytoplasm that recognize the nonself signatures of viral RNAs to trigger IFN responses.

6. Knockdown of PBRM1 (show PBRM1 Proteins) in colon cancer cells increased the expression of two receptor genes (RIG-I and MDA5 (show IFIH1 Proteins)) and upregulated interferon (show IFNA Proteins) (IFN)-related and inflammation-related gene signatures.

7. Dengue virus infection of human dendritic cells drives follicular T helper cells formation via crosstalk of RIG-I and MDA5 (show IFIH1 Proteins).

8. DDX58_rs10813831 T-allele may be associated with a reduced risk of nodular sclerosis EBV-related cHL (show CHRDL1 Proteins), which suggests a role for RIG-I (retinoic acid-inducible gene I), encoded by DDX58, in these cases.

9. mutations in the genes encoding for RIG-I and MDA5 (show IFIH1 Proteins) have been identified to cause rare diseases including Aicardi-Goutieres syndrome, Systemic Lupus Erythematosus in certain individuals as well as classic and atypical Singleton-Merten syndrome. Patients carrying mono-allelic mutations in MDA5 (show IFIH1 Proteins) and RIG-I show constitutive activation of the RIG-I receptors and downstream signalling

10. These findings demonstrate how IFNgamma induced CK2 (show CSNK2A1 Proteins) regulates RIG-I to drive a complex program of metabolic adaptation and redox homeostasis, crucial for determining glioma cell fate.

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

1. RNF122 (show RNF122 Proteins) suppresses antiviral type I interferon (show IFNA Proteins) production by targeting RIG-I caspase (show CASP3 Proteins) activation and recruitment domains to mediate RIG-I degradation.

2. innate immune signaling mediated by RLR (show DHX58 Proteins) plays a critical role in nuclear reprogramming.

3. RIG-I expression is markedly increased in the affected skin derived from psoriasis patients and from both IL-23 (show IL23A Proteins)- and imiquimod -induced psoriasis-like mouse model.

4. 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.

5. Collectively, these results uncover an independent functional contribution of the apo (show C9orf3 Proteins)-Rig-I/Stat3 (show STAT3 Proteins) interaction in the maintenance of Treg/Th17 cell balance.

6. The RIG-I, as well as the adaptor protein mitochondrial antiviral signaling protein (show MAVS Proteins), regulates NF-kappaB (show NFKB1 Proteins)-mediated induction of adhesion molecules and proinflammatory cytokine expression in response to LPS (show TLR4 Proteins).

7. Data suggest that activation of either RIG-I/MAVS (show MAVS Proteins) or STING pathways during acute intestinal tissue injury in mice resulted in IFN-I signaling that maintained gut (show GUSB Proteins) epithelial barrier integrity and reduced GVHD severity.

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

9. identifies DDX58 and MTHFSD as two TDP-43 (show TARDBP Proteins) targets that are misregulated in amyotrophic lateral sclerosis. 1

10. Data show that preconditioning with poly(I:C) alters toll (show TLR4 Proteins)-like receptors (TLR) and RIG-I-like receptors (RLRs) responses in opposite directions.

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

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

2. These data indicate that classical swine fever virus can be recognized by both RIG-I and MDA5 (show IFIH1 Proteins) to initiate the RIG-I signaling pathway to trigger innate defenses against infection.

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