Evidence map›Paper›PMID 20106928›Full record

ArticleJournal of virology2010

Stable formation of compositionally unique stress granules in virus-infected cells.

Joanna Piotrowska, Spencer J Hansen, Nogi Park, Katarzyna Jamka, Peter Sarnow, Kurt E Gustin

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

84 citing papers in PubMed, 118 citations in OpenAlex.

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  20. A proposed role for the SARS-CoV-2 nucleocapsid protein in the formation and regulation of biomolecular condensates.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article

24 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

6 authors at 3 institutions in 1 country.

Joanna PiotrowskaUniversity of Arizona College of Medicine-Phoenix, Department of Basic Medical Sciences, 425 N. Fifth Street, ABC1 Room 328, Phoenix, AZ 85004, USA.
Spencer J Hansen
Nogi Park
Katarzyna Jamka
Peter Sarnow
Kurt E Gustin
University of Arizona · USUniversity of Idaho · USStanford University · US

Funding

UNDERGRADUATE COLLEGE OUTREACH PROGRAMP20RR016454 · NCRR · UNIVERSITY OF IDAHO · PI CHASE, JENNIFER R · 2001 to 2011
$35.3M
TRANSCRIPTIONAL ATTENUATION OF THE TYPE I INTERFERON RESPONSE BY RHINOVIRUSP20RR015587 · NCRR · UNIVERSITY OF IDAHO · PI BOHACH, GREGORY A · 2000 to 2009
$19.0M
Inhibition of the dsRNA Response by PicornavirusesR56AI064432 · NIAID · UNIVERSITY OF IDAHO · PI GUSTIN, KURT E · 2007 to 2007
$339k
NCRR NIH HHS P20 RR015587NCRR NIH HHS P20 RR016454NCRR NIH HHS P20 RR15587NIAID NIH HHS AI064432NIAID NIH HHS R56 AI064432
6 · The paper itself

Abstract

Stress granules are sites of mRNA storage formed in response to a variety of stresses, including viral infections. Here, the mechanisms and consequences of stress granule formation during poliovirus infection were examined. The results indicate that stress granules containing T-cell-restricted intracellular antigen 1 (TIA-1) and mRNA are stably constituted in infected cells despite lacking intact RasGAP SH3-domain binding protein 1 (G3BP) and eukaryotic initiation factor 4G. Fluorescent in situ hybridization revealed that stress granules in infected cells do not contain significant amounts of viral positive-strand RNA. Infection does not prevent stress granule formation in response to heat shock, indicating that poliovirus does not block de novo stress granule formation. A mutant TIA-1 protein that prevents stress granule formation during oxidative stress also prevents formation in infected cells. However, stress granule formation during infection is more dependent upon ongoing transcription than is formation during oxidative stress or heat shock. Furthermore, Sam68 is recruited to stress granules in infected cells but not to stress granules formed in response to oxidative stress or heat shock. These results demonstrate that stress granule formation in poliovirus-infected cells utilizes a transcription-dependent pathway that results in the appearance of stable, compositionally unique stress granules.

Indexed as

Cytoplasmic GranulesEukaryotic Initiation Factor-2Heat-Shock ProteinsHeat-Shock ResponseHeLa CellsHSP27 Heat-Shock ProteinsHumansMolecular ChaperonesPhosphorylationPoliovirusPoly(A)-Binding ProteinsRNA, MessengerT-Cell Intracellular Antigen-1Transcription, GeneticEukaryotic Initiation Factor-2Heat-Shock ProteinsHSP27 Heat-Shock ProteinsHSPB1 protein, humanMolecular ChaperonesPoly(A)-Binding ProteinsRNA, MessengerT-Cell Intracellular Antigen-1TIA1 protein, human

Identifiers

PMID20106928
PMCPMC2838110
OpenAlexW2038822504

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.