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PXD011577

DataSet Summary

  • HostingRepository: PRIDE
  • AnnounceDate: 2018-11-07
  • AnnouncementXML: Submission_2018-11-07_06:16:40.xml
  • DigitalObjectIdentifier:
  • ReviewLevel: Peer-reviewed dataset
  • DatasetOrigin: Original data
  • RepositorySupport: Unsupported dataset by repository
  • PrimarySubmitter: Bin Zhou
  • Title: lnc-EAPV binding proteins in C57BL/6J BMDMs
  • Description: Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.
  • SpeciesList: scientific name: Mus musculus (Mouse); NCBI TaxID: 10090;
  • ModificationList: monohydroxylated residue; iodoacetamide derivatized residue
  • Instrument: LTQ Orbitrap Elite

Dataset History

VersionDatetimeStatusChangeLog Entry
02018-11-05 02:30:44ID requested
12018-11-07 06:16:41announced

Publication List

  1. Dataset with its publication pending

Keyword List

  1. submitter keyword: lnc-EPAV;RBP;BMDMs

Contact List

    Feng Qian
    • contact affiliation: School of Life Sciences Fudan University
    • contact email: fengqian@fudan.edu.cn
    • lab head:
    Bin Zhou
    • contact affiliation: School of Life Sciences Fudan University
    • contact email: zhoubin1999fd@163.com
    • dataset submitter:

Full Dataset Link List

  1. Dataset FTP location
  2. PRIDE project URI
Repository Record List
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