Topic
NSP1
About: NSP1 is a research topic. Over the lifetime, 248 publications have been published within this topic receiving 12044 citations.
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TL;DR: It is demonstrated that nsp1β has ability to inhibit both interferon synthesis and signaling, while nSp1α alone strongly inhibits interferons synthesis.
166 citations
TL;DR: Current knowledge about the biological functions of CoV nsp1 is summarized that provides an insight into the novel strategies utilized by this viral protein to modulate host and viral gene expression during CoV infection.
163 citations
TL;DR: Targeted degradation of an F-box protein of an E3 ligase complex with a prominent role in modulation of innate immune signaling and cell proliferation pathways is a unique mechanism of IFN antagonism and defines a second strategy of immune evasion used by rotaviruses.
Abstract: Mechanisms by which viruses counter innate host defense responses generally involve inhibition of one or more components of the interferon (IFN) system. Multiple steps in the induction and amplification of IFN signaling are targeted for inhibition by viral proteins, and many of the IFN antagonists have direct or indirect effects on activation of latent cytoplasmic transcription factors. Rotavirus nonstructural protein NSP1 blocks transcription of type I IFNα/β by inducing proteasome-dependent degradation of IFN-regulatory factors 3 (IRF3), IRF5, and IRF7. In this study, we show that rotavirus NSP1 also inhibits activation of NFκB and does so by a novel mechanism. Proteasome-mediated degradation of inhibitor of κB (IκBα) is required for NFκB activation. Phosphorylated IκBα is a substrate for polyubiquitination by a multisubunit E3 ubiquitin ligase complex, Skp1/Cul1/F-box, in which the F-box substrate recognition protein is β-transducin repeat containing protein (β-TrCP). The data presented show that phosphorylated IκBα is stable in rotavirus-infected cells because infection induces proteasome-dependent degradation of β-TrCP. NSP1 expressed in isolation in transiently transfected cells is sufficient to induce this effect. Targeted degradation of an F-box protein of an E3 ligase complex with a prominent role in modulation of innate immune signaling and cell proliferation pathways is a unique mechanism of IFN antagonism and defines a second strategy of immune evasion used by rotaviruses.
161 citations
TL;DR: PEDV modulates the host innate immune responses by degrading CBP and suppressing ISGs expression and it is demonstrated that the CBP degradation by nsp1 was proteasome-dependent.
137 citations
TL;DR: In this paper, the virulence factor Nsp1 protein of SARS-CoV-2 interacts with the host mRNA export receptor heterodimer NXF1-NXT1, which is responsible for nuclear export of cellular mRNAs.
Abstract: The ongoing unprecedented severe acute respiratory syndrome caused by the SARS-CoV-2 outbreak worldwide has highlighted the need for understanding viral-host interactions involved in mechanisms of virulence Here, we show that the virulence factor Nsp1 protein of SARS-CoV-2 interacts with the host messenger RNA (mRNA) export receptor heterodimer NXF1-NXT1, which is responsible for nuclear export of cellular mRNAs Nsp1 prevents proper binding of NXF1 to mRNA export adaptors and NXF1 docking at the nuclear pore complex As a result, a significant number of cellular mRNAs are retained in the nucleus during infection Increased levels of NXF1 rescues the Nsp1-mediated mRNA export block and inhibits SARS-CoV-2 infection Thus, antagonizing the Nsp1 inhibitory function on mRNA export may represent a strategy to restoring proper antiviral host gene expression in infected cells
135 citations