Evidence map›Paper›PMID 31270230›Full record

ArticleJournal of virology2019

The Guanine Nucleotide Exchange Factor GBF1 Participates in Rotavirus Replication.

José L Martínez, Francesca Arnoldi, Elisabeth M Schraner, Catherine Eichwald, Daniela Silva-Ayala, Eunjoo Lee, Elizabeth Sztul, Óscar R Burrone, Susana López, Carlos F Arias

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Exosomal transmission of viruses, a two-edged biological sword.Cell communication and signaling : CCS · 2023
    Review
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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

10 authors at 5 institutions in 4 countries.

José L MartínezInstituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, México.ORCID 0000-0002-0529-7558
Francesca ArnoldiInternational Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Elisabeth M SchranerInstitute of Virology, University of Zurich, Zurich, Switzerland.
Catherine EichwaldInstitute of Virology, University of Zurich, Zurich, Switzerland.
Daniela Silva-AyalaInstituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, México.
Eunjoo LeeDepartment of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Elizabeth SztulDepartment of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Óscar R BurroneInternational Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Susana LópezInstituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, México.
Carlos F AriasInstituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, México arias@ibt.unam.mx.ORCID 0000-0003-3130-4501
Universidad Nacional Autónoma de México · MXUniversity of Alabama at Birmingham · USUniversity of Zurich · CHInternational Centre for Genetic Engineering and Biotechnology · ITUniversity of Trieste · IT

Funding

Spatio-temporal regulation of ARF signaling in vesicle formationR01GM122802 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SZTUL, ELIZABETH S · 2017 to 2020
$1.5M
NIGMS NIH HHS R01 GM122802
6 · The paper itself

Abstract

Cellular and viral factors participate in the replication cycle of rotavirus. We report that the guanine nucleotide exchange factor GBF1, which activates the small GTPase Arf1 to induce COPI transport processes, is required for rotavirus replication since knocking down GBF1 expression by RNA interference or inhibiting its activity by treatment with brefeldin A (BFA) or Golgicide A (GCA) significantly reduces the yield of infectious viral progeny. This reduction in virus yield was related to a block in virus assembly, since in the presence of either BFA or GCA, the assembly of infectious mature triple-layered virions was significantly prevented and only double-layered particles were detected. We report that the catalytic activity of GBF1, but not the activation of Arf1, is essential for the assembly of the outer capsid of rotavirus. We show that both BFA and GCA, as well as interfering with the synthesis of GBF1, alter the electrophoretic mobility of glycoproteins VP7 and NSP4 and block the trimerization of the virus surface protein VP7, a step required for its incorporation into virus particles. Although a posttranslational modification of VP7 (other than glycosylation) could be related to the lack of trimerization, we found that NSP4 might also be involved in this process, since knocking down its expression reduces VP7 trimerization. In support, recombinant VP7 protein overexpressed in transfected cells formed trimers only when cotransfected with NSP4.

Indexed as

Host-Pathogen InteractionsVirus AssemblyVirus ReplicationADP-Ribosylation Factor 1AnimalsCell LineEnzyme InhibitorsGene Knockdown TechniquesGuanine Nucleotide Exchange FactorsHumansMacaca mulattaRotavirusViral LoadViral ProteinsADP-Ribosylation Factor 1ARF1 protein, humanEnzyme InhibitorsGBF1 protein, humanGuanine Nucleotide Exchange FactorsViral ProteinsGBF1 nucleotide exchange factormorphogenesisrotavirus

Identifiers

PMID31270230
PMCPMC6744240
OpenAlexW2955303739

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.