Negative Regulation of RIG-I-Mediated Innate Antiviral Signaling by SEC14L1

Li, Meng-Tong; Di, Wei; Xu, Hao; Yang, Yongkang; Chen, Haiwei; Zhang, Feixiong; Zhai, Zhonghe; Chen, Danying

doi:10.1128/jvi.01073-13

Cited by 38 publications

(29 citation statements)

References 43 publications

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“…In addition, IFN-induced ISG15 negatively regulates the RIG-I mediated signaling in a feedback-loop control manner (80). SEC14L1 has been observed competing with MAVS for RIG-I CARD binding (81). Furthermore, autophagy has been reported to be involved in RIG-I modulation through its key regulator, the Atg5-Atg12 conjugate.…”

Section: Other Regulatory Mechanismsmentioning

confidence: 99%

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

2017

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Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patterns via pattern-recognition receptors is essential for the host to mount defensive and protective responses. Retinoic acid-inducible gene-I (RIG-I) is critical in triggering antiviral and inflammatory responses for the control of viral replication in response to cytoplasmic virus-specific RNA structures. Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade that coordinates the induction of type I interferons (IFNs), as well as a large variety of antiviral interferon-stimulated genes. The RIG-I activation is tightly regulated via various posttranslational modifications for the prevention of aberrant innate immune signaling. By contrast, viruses have evolved mechanisms of evasion, such as sequestrating viral structures from RIG-I detections and targeting receptor or signaling molecules for degradation. These virus–host interactions have broadened our understanding of viral pathogenesis and provided insights into the function of the RIG-I pathway. In this review, we summarize the recent advances regarding RIG-I pathogen recognition and signaling transduction, cell-intrinsic control of RIG-I activation, and the viral antagonism of RIG-I signaling.

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Section: Other Regulatory Mechanismsmentioning

confidence: 99%

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

2017

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“…SEC14L1, a member of the SEC14 family, appears to negatively regulate RIG‐I signaling by associating specifically with the RIG‐I N‐terminal CARDs (Fig. ).…”

Section: Negative Regulation Of Rig‐imentioning

confidence: 99%

“…By interacting with the CARDs, SEC14L1 directly competes with MAVS for binding to RIG‐I. Co‐expression of SEC14L1 with RIG‐I or constitutively active N‐RIG‐I in HEK293T cells resulted in decreased RIG‐I signaling, whereas gene silencing of SEC14L1 resulted in enhanced signaling . Co‐expression of SEC14L1 in HEK293T cells prevented the interaction of RIG‐I and MAVS in a dose‐dependent manner, thus inhibiting downstream signaling.…”

Section: Negative Regulation Of Rig‐imentioning

confidence: 99%

Negative regulators of the RIG‐I‐like receptor signaling pathway

2017

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SUMMARY Upon recognition of specific molecular patterns on viruses, bacteria and fungi, host cells trigger an innate immune response, which culminates in the production of type I interferons (IFN), pro-inflammatory cytokines and chemokines, and restricts pathogen replication and spread within the host. At each stage of the immune response, there are stimulatory and inhibitory signals that regulate the magnitude, quality, and character of the response. Positive regulation promotes an antiviral state to control and eventually clear infection whereas negative regulation dampens inflammation and prevents immune-mediated tissue damage. An over-exuberant innate immune response can lead to the destruction of cells and tissues, and the development of spontaneous autoimmunity. The RIG-I-like receptors (RLRs) retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) belong to a family of cytosolic host RNA helicases that recognize distinct non-self RNA signatures and trigger innate immune responses against several RNA virus infections. The RLR signaling pathway is tightly regulated to achieve a well-orchestrated response aimed at maximizing antiviral immunity and minimizing immune-mediated pathology. This review highlights contemporary findings on negative regulators of the RLR signaling pathway, with specific focus on the proteins and biological processes that directly regulate RIG-I, MDA5 and MAVS function.

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“…Another cellular protein that has been reported to antagonize antiviral signaling by inhibiting the interaction between RIG-I and MAVS is the autophagy-regulatory protein conjugate Atg5-Atg12, which binds to the CARDs of both RIG-I and MAVS, thereby preventing their interaction and downstream signaling [96]. The proteins SEC14L1 and NLRC5 have been shown to interact with the CARDs of RIG-I and/or MDA5, competing with RLR binding to MAVS [97,98]. Furthermore, the ubiquitin-regulatory-X-domain-containing protein 1 (UBXN1) was found to be relocalized to mitochondria upon viral infection, where it competes with the signalosome proteins TRAF3 and TRAF6 for binding to MAVS [99].…”

Section: Regulation Of Mda5mentioning

confidence: 99%

Regulation of RIG-I-like receptor signaling by host and viral proteins

Chiang

Davis

Gack

2014

Cytokine & Growth Factor Reviews

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Vertebrate innate immunity is characterized by an effective immune surveillance apparatus, evolved to sense foreign structures, such as proteins or nucleic acids of invading microbes. RIG-I-like receptors (RLRs) are key sensors of viral RNA species in the host cell cytoplasm. Activation of RLRs in response to viral RNA triggers an antiviral defense program through the production of hundreds of antiviral effector proteins including cytokines, chemokines, and host restriction factors that directly interfere with distinct steps in the virus life cycle. To avoid premature or abnormal antiviral and proinflammatory responses, which could have harmful consequences for the host, the signaling activities of RLRs and their common adaptor molecule, MAVS, are delicately controlled by cell-intrinsic regulatory mechanisms. Furthermore, viruses have evolved multiple strategies to modulate RLR-MAVS signal transduction to escape from immune surveillance. Here, we summarize recent progress in our understanding of the regulation of RLR signaling through host factors and viral antagonistic proteins.

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Negative Regulation of RIG-I-Mediated Innate Antiviral Signaling by SEC14L1

Cited by 38 publications

References 43 publications

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

Negative regulators of the RIG‐I‐like receptor signaling pathway

Regulation of RIG-I-like receptor signaling by host and viral proteins

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