Evidence map›Paper›PMID 28248290›Full record

ArticleNature microbiology2017

Systems-based analysis of RIG-I-dependent signalling identifies KHSRP as an inhibitor of RIG-I receptor activation.

Stephen Soonthornvacharin, Ariel Rodriguez-Frandsen, Yingyao Zhou, Felipe Galvez, Nicholas J Huffmaster, Shashank Tripathi, Vinod R M T Balasubramaniam, Atsushi Inoue, Elisa de Castro, Hong Moulton and 9 more

Abstract read
In one paragraph

Article in Nature microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Cross Talk between MicroRNAs and Dengue Virus.The American journal of tropical medicine and hygiene · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. The lncRNAs involved in regulating the RIG-I signaling pathway.Frontiers in cellular and infection microbiology · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Mitochondrial Interactome: A Focus on Antiviral Signaling Pathways.Frontiers in cell and developmental biology · 2020
    Review
  17. Article
  18. Intracellular sensing of viral genomes and viral evasion.Experimental & molecular medicine · 2019
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 2 countries.

Stephen SoonthornvacharinImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Ariel Rodriguez-FrandsenImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.ORCID http://orcid.org/0000-0001-6850-5003
Yingyao ZhouGenomics Institute of the Novartis Research Foundation, 10675 John Jay Hopkins Drive, San Diego, California 92121, USA.
Felipe GalvezImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Nicholas J HuffmasterImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Shashank TripathiDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, New York 10029, USA.
Vinod R M T BalasubramaniamDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, New York 10029, USA.
Atsushi InoueImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Elisa de CastroDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, New York 10029, USA.
Hong MoultonDepartment of Biomedical Sciences, College of Veterinary Medicine, Oregon State University Corvallis, 450 SW 30th Street, Oregon 97331, USA.
David A SteinDepartment of Biomedical Sciences, College of Veterinary Medicine, Oregon State University Corvallis, 450 SW 30th Street, Oregon 97331, USA.
María Teresa Sánchez-AparicioDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, New York 10029, USA.
Paul D De JesusImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Quy NguyenImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Renate KönigImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Nevan J KroganDepartment of Cellular and Molecular Pharmacology, University of California San Francisco, 1700 4th Street, Byers Hall 308D, Box 2530, San Francisco, California 94158, USA.
Adolfo García-SastreDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, New York 10029, USA.
Sunnie M YohImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Sumit K ChandaImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.
Sanford Burnham Prebys Medical Discovery Institute · USIcahn School of Medicine at Mount Sinai · USDiscovery Institute · USOregon State University · USGenomics Institute of the Novartis Research Foundation · USUniversity of California, San Francisco · US

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Michael Jackson · 1985 to 2026
$107.2M
Virus CoreU19AI106754 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ALBRECHT, RANDY A. · 2013 to 2017
$26.0M
SYNTHETIC SYSTEMSP50GM085764 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HASTY, JEFF M, IDEKER, TREY · 2010 to 2018
$23.3M
NCI NIH HHS P30 CA030199NIAID NIH HHS HHSN272201400008CNIAID NIH HHS U19 AI106754NIGMS NIH HHS P50 GM085764
6 · The paper itself

Abstract

Retinoic acid-inducible gene I (RIG-I) receptor recognizes 5'-triphosphorylated RNA and triggers a signalling cascade that results in the induction of type-I interferon (IFN)-dependent responses. Its precise regulation represents a pivotal balance between antiviral defences and autoimmunity. To elucidate the cellular cofactors that regulate RIG-I signalling, we performed two global RNA interference analyses to identify both positive and negative regulatory nodes operating on the signalling pathway during virus infection. These factors were integrated with experimentally and computationally derived interactome data to build a RIG-I protein interaction network. Our analysis revealed diverse cellular processes, including the unfolded protein response, Wnt signalling and RNA metabolism, as critical cellular components governing innate responses to non-self RNA species. Importantly, we identified K-Homology Splicing Regulatory Protein (KHSRP) as a negative regulator of this pathway. We find that KHSRP associates with the regulatory domain of RIG-I to maintain the receptor in an inactive state and attenuate its sensing of viral RNA (vRNA). Consistent with increased RIG-I antiviral signalling in the absence of KHSRP, viral replication is reduced when KHSRP expression is knocked down both in vitro and in vivo. Taken together, these data indicate that KHSRP functions as a checkpoint regulator of the innate immune response to pathogen challenge.

Indexed as

Signal TransductionDEAD Box Protein 58HEK293 CellsHumansImmunity, InnateInfluenza A Virus, H1N1 SubtypeProtein BindingProtein Interaction MappingProtein Interaction MapsReceptors, ImmunologicRNA-Binding ProteinsRNA, ViralTrans-ActivatorsDEAD Box Protein 58KHSRP protein, humanReceptors, ImmunologicRIGI protein, humanRNA-Binding ProteinsRNA, ViralTrans-Activators

Identifiers

PMID28248290
PMCPMC5338947
OpenAlexW2593581914

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.