Targeting nuclear proteins for control of viral replication

Meng, Wen; Wang, Xiao-Jia; Wang, Hwa‐Chain Robert

doi:10.1080/1040841x.2018.1553848

Cited by 6 publications

(5 citation statements)

References 199 publications

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“…Another way in which flaviviruses, especially HCV, evade the immune system is to replicate in membrane-delimited vesicles in the cytoplasm, termed viral factories ( 210 ). These structures prevent the detection of viral genomes by various innate immune pathways.…”

Section: Flavivirusesmentioning

confidence: 99%

Crosstalk between nucleocytoplasmic trafficking and the innate immune response to viral infection

Shen

Wang

Palazzo

2021

Journal of Biological Chemistry

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The nuclear pore complex is the sole gateway connecting the nucleoplasm and cytoplasm. In humans, the nuclear pore complex is one of the largest multiprotein assemblies in the cell, with a molecular mass of ∼110 MDa and consisting of 8 to 64 copies of about 34 different nuclear pore proteins, termed nucleoporins, for a total of 1000 subunits per pore. Trafficking events across the nuclear pore are mediated by nuclear transport receptors and are highly regulated. The nuclear pore complex is also used by several RNA viruses and almost all DNA viruses to access the host cell nucleoplasm for replication. Viruses hijack the nuclear pore complex, and nuclear transport receptors, to access the nucleoplasm where they replicate. In addition, the nuclear pore complex is used by the cell innate immune system, a network of signal transduction pathways that coordinates the first response to foreign invaders, including viruses and other pathogens. Several branches of this response depend on dynamic signaling events that involve the nuclear translocation of downstream signal transducers. Mounting evidence has shown that these signaling cascades, especially those steps that involve nucleocytoplasmic trafficking events, are targeted by viruses so that they can evade the innate immune system. This review summarizes how nuclear pore proteins and nuclear transport receptors contribute to the innate immune response and highlights how viruses manipulate this cellular machinery to favor infection. A comprehensive understanding of nuclear pore proteins in antiviral innate immunity will likely contribute to the development of new antiviral therapeutic strategies.

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Section: Flavivirusesmentioning

confidence: 99%

Crosstalk between nucleocytoplasmic trafficking and the innate immune response to viral infection

Shen

Wang

Palazzo

2021

Journal of Biological Chemistry

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“…Notably, all the four proteins analyzed by immunofluorescence staining, including the nuclear transcription factors HELZ2 and RXRG localize in the cytoplasm of infected cells ( Figure 5). This is not surprising, as virus infections are known to perturb the spatio-temporal organization of cellular proteins and flaviviruses recruit nuclear proteins to the cytoplasm to aid in viral replication and evade host immune sensing [57,58]. Nonetheless, the overlapping localization pattern FGR, APOC3, HELZ2 and RXRG with the ZIKV Envelope protein and the known cytoplasmic nature of ZIKV life cycle [59], makes it tempting to speculate that these proteins could have important roles in modulating ZIKV life cycle.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of Ephrin receptor and PPAR signaling pathways in neural progenitor cells infected by Zika virus

Raman

Latreille

Gao

et al. 2020

Emerging Microbes & Infections

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Zika virus (ZIKV) infection is a serious public threat with cases reported in about 70 countries and territories. One of the most serious consequences of ZIKV infection is congenital microcephaly in babies. Congenital microcephaly has been suggested to result from infection of neural progenitor cells (NPCs) in the developing fetal brain. However, the molecular and cellular mechanisms underlying microcephaly development remains to be fully elucidated. In this study, we employed quantitative proteomics to determine protein expression profile that occur during viral replication in NPCs. Bioinformatics analysis of the protein expression changes resulted in the identification of a wide range of cell signaling pathways. Specifically, pathways involved in neurogenesis and embryonic development were markedly altered, along with those associated with cell cycle, apoptosis, lipid metabolism and oxidative stress. Notably, the differential regulation of Ephrin Receptor and PPAR signaling pathways, as revealed by quantitative proteomics and validated by qPCR array, underscores the need to explore these pathways in disease development. Collectively, these results indicate that ZIKV-induced pathogenesis involves complex virus-host reactions; the findings reported here could help shed light on the mechanisms underlying ZIKV-induced microcephaly and ZIKV replication in NPCs.

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“…Like VACV, HCV replicate in viral factories [ 121 , 164 ]. These contain nuclear pore-like structures, which consist of RanBP2, Nup153, Nup155, Nup98, and Nup53.…”

Section: The Interplay Between Ranbp2 and Virusesmentioning

confidence: 99%

Roles of Nucleoporin RanBP2/Nup358 in Acute Necrotizing Encephalopathy Type 1 (ANE1) and Viral Infection

Jiang

Wang

Palazzo

et al. 2022

IJMS

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Ran Binding Protein 2 (RanBP2 or Nucleoporin358) is one of the main components of the cytoplasmic filaments of the nuclear pore complex. Mutations in the RANBP2 gene are associated with acute necrotizing encephalopathy type 1 (ANE1), a rare condition where patients experience a sharp rise in cytokine production in response to viral infection and undergo hyperinflammation, seizures, coma, and a high rate of mortality. Despite this, it remains unclear howRanBP2 and its ANE1-associated mutations contribute to pathology. Mounting evidence has shown that RanBP2 interacts with distinct viruses to regulate viral infection. In addition, RanBP2 may regulate innate immune response pathways. This review summarizes recent advances in our understanding of how mutations in RANBP2 contribute to ANE1 and discusses how RanBP2 interacts with distinct viruses and affects viral infection. Recent findings indicate that RanBP2 might be an important therapeutic target, not only in the suppression of ANE1-driven cytokine storms, but also to combat hyperinflammation in response to viral infections.

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Targeting nuclear proteins for control of viral replication

Cited by 6 publications

References 199 publications

Crosstalk between nucleocytoplasmic trafficking and the innate immune response to viral infection

Crosstalk between nucleocytoplasmic trafficking and the innate immune response to viral infection

Dysregulation of Ephrin receptor and PPAR signaling pathways in neural progenitor cells infected by Zika virus

Roles of Nucleoporin RanBP2/Nup358 in Acute Necrotizing Encephalopathy Type 1 (ANE1) and Viral Infection

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