Evidence map›Paper›PMID 27595182›Full record

ReviewCytokine2020

New advances in our understanding of the "unique" RNase L in host pathogen interaction and immune signaling.

Elona Gusho, Danika Baskar, Shuvojit Banerjee

Open access · greenAbstract readReview
In one paragraph

Review in Cytokine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 25% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  7. A CRISPR-Cas9 knockout screening identifies IRF2 as a key driver of OAS3/RNase L-mediated RNA decay during viral infection.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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

3 authors at 2 institutions in 1 country.

Elona GushoDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue Cleveland, OH 44195, USA.
Danika BaskarDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue Cleveland, OH 44195, USA; Pediatrics Division Office, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA(1).
Shuvojit BanerjeeDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue Cleveland, OH 44195, USA. Electronic address: banerjs2@ccf.org.
Cleveland Clinic Lerner College of Medicine · USCleveland Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ever since the discovery of the existence of an interferon (IFN)-regulated ribonuclease, significant advances have been made in understanding the mechanism and associated regulatory effects of its action. What had been studied initially as a "unique" endoribonuclease is currently known as ribonuclease L (RNase L where "L" stands for latent). Some of the key developments include discovery of the RNase L signaling pathway, its structural characterization, and its molecular cloning. RNase L has been implicated in antiviral and antibacterial defense, as well as in hereditary prostate cancer. RNase L is activated by 2'-5' linked oligoadenylates (2-5A), which are synthesized by the oligoadenylate synthetases (OASs), a family of IFN-regulated pathogen recognition receptors that sense double-stranded RNAs. Activated RNase L cleaves single stranded RNAs, including viral RNAs and cellular RNAs. The catalytic activity of RNase L has been found to lead into the activation of several cellular signaling pathways, including those involved in autophagy, apoptosis, IFN-β production, NLRP3 inflammasome activation leading to IL-1β secretion, inhibition of cell migration, and cell adhesion. In this review, we will highlight the newest advances in our understanding of the catalytic role of RNase L in the context of different cellular pathways and extend the scope of these findings to discussion of potential therapeutic targets for antimicrobial drug development.

Indexed as

AnimalsEndoribonucleasesHost-Pathogen InteractionsHumansImmunityInterferonsSignal Transduction2-5A-dependent ribonucleaseEndoribonucleasesInterferons2′-5′ PhosphodiesteraseAutophagyCell migrationInflammasomeInfluenza A virusInnate immunityOligoadenylate synthetaseRibonuclease L

Identifiers

PMID27595182
PMCPMC7128181
OpenAlexW2518253722

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.