Evidence map›Paper›PMID 19028691›Full record

ArticleThe Journal of biological chemistry2009

The RNA-activated protein kinase enhances the induction of interferon-beta and apoptosis mediated by cytoplasmic RNA sensors.

Christopher S McAllister, Charles E Samuel

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

64 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Plant physiology · 2020
    Article
  6. RNA Signaling in Pulmonary Arterial Hypertension-A Double-Stranded Sword.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Christopher S McAllisterDepartment of Molecular, Cellular and Developmental Biology, University of California, Santa Barbara, California 93106, USA.
Charles E Samuel
University of California, Santa Barbara · US

Funding

INTERFERON ACTION AND PROTEIN PHOSPHORYLATIONR01AI020611 · NIAID · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI SAMUEL, CHARLES E · 1985 to 2014
$3.4M
MECHANISM OF INTERFERON ACTIONR01AI012520 · NIAID · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI SAMUEL, CHARLES E · 1985 to 2009
$3.1M
MECHANISM OF INTERFERON ACTIONR37AI012520 · NIAID · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI SAMUEL, CHARLES E. · 1989 to 1998
–
NIAID NIH HHS AI-12520NIAID NIH HHS AI-20611
6 · The paper itself

Abstract

Detection of foreign RNA by the innate immune system can trigger the induction of type I interferon (IFN) and apoptosis. Important antiviral defense pathways that result in type I IFN production following the recognition of foreign double-stranded RNA (dsRNA) include the RIG-I family helicases and IPS-1 adaptor cytosolic pathway and the Toll-like receptor 3 and TIR domain-containing adaptor-inducing IFN-beta (TRIF) adaptor membrane-associated pathway, both of which activate IFN regulatory factor 3 (IRF3). In addition to triggering an innate immune response, dsRNAs are widely used to mediate gene-selective silencing in mammalian cells by the RNA interference pathway. We investigated the ability of short interfering RNAs, including T7 phage polymerase-synthesized RNA (PRNA), which like some viral RNAs contains a 5'-triphosphate, to selectively silence gene expression and to cause induction of IFN-beta and apoptosis. We found that PRNA-mediated gene silencing and associated nonspecific pro-apoptotic and IFN-inducing effects were dependent on the cell line and RNA length. Double-stranded PRNAs 50 nucleotides long as well as polyinosinic-polycytidylic acid activated the RNA-dependent protein kinase (PKR) and induced significant levels of IFN-beta and apoptosis, whereas shorter PRNAs and chemically synthesized dsRNAs did not. Effector caspase activation and apoptosis following RNA transfection was enhanced by pretreatment with IFN, and removal of the 5'-phosphate from PRNAs decreased induction of both IFN-beta and apoptosis. PKR, in addition to IPS-1 and IRF3 but not TRIF, was required for maximal type I IFN-beta induction and the induction of apoptosis by both transfected PRNAs and polyinosinic-polycytidylic acid.

Indexed as

Adaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportAnimalsApoptosisCaspasesCHO CellsCricetinaeCricetuluseIF-2 KinaseGene SilencingHeLa CellsHumansImmunity, InnateInterferon-betaInterferon Regulatory Factor-3MiceAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportCaspaseseIF-2 KinaseInterferon-betaInterferon Regulatory Factor-3IRF3 protein, humanIrf3 protein, mouseMAVS protein, humanMAVS protein, mousePoly I-CRNA, Double-StrandedTICAM1 protein, humanTicam1 protein, mouseTLR3 protein, humanTLR3 protein, mouseToll-Like Receptor 3

Identifiers

PMID19028691
PMCPMC2615529
OpenAlexW1976117598

What OpenQuestion holds

Textmetadata
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.