Evidence map›Paper›PMID 26582347›Full record

ArticleScientific reports2015

Slit2N Inhibits Transmission of HIV-1 from Dendritic Cells to T-cells by Modulating Novel Cytoskeletal Elements.

Ashutosh Shrivastava, Anil Prasad, Paula M Kuzontkoski, Jinlong Yu, Jerome E Groopman

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Article
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  8. Review
  9. Specialized Intercellular Communications via Cytonemes and Nanotubes.Annual review of cell and developmental biology · 2018
    Review
  10. Review
  11. Review
  12. Distinct functions of diaphanous-related formins regulate HIV-1 uncoating and transport.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  13. Article
  14. Review
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

5 authors at 3 institutions in 1 country.

Ashutosh ShrivastavaDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Anil PrasadDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Paula M KuzontkoskiDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Jinlong YuDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Jerome E GroopmanDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Beth Israel Deaconess Medical Center · USHarvard University · USEBSCO Industries (United States) · US

Funding

Novel Strategies to Antagonize Cocaine-Enhanced HIV PathobiologyR01DA036298 · NIDA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI GROOPMAN, JEROME E, MEMPEL, THORSTEN ROMAN · 2013 to 2017
$2.0M
NIDA NIH HHS R01 DA036298NIDA NIH HHS R01DA036298
6 · The paper itself

Abstract

Dendritic cells are among the first cells to encounter sexually acquired human immunodeficiency virus (HIV-1), in the mucosa, and they can transmit HIV-1 to CD4(+) T-cells via an infectious synapse. Recent studies reveal that actin-rich membrane extensions establish direct contact between cells at this synapse and facilitate virus transmission. Genesis of these contacts involves signaling through c-Src and Cdc42, which modulate actin polymerization and filopodia formation via the Arp2/3 complex and Diaphanous 2 (Diaph2). We found that Slit2N, a ligand for the Roundabout (Robo) receptors, blocked HIV-1-induced signaling through Arp2/3 and Diaph2, decreased filopodial extensions on dendritic cells, and inhibited cell-to-cell transmission of HIV-1 in a Robo1-dependent manner. Employing proteomic analysis, we identified Flightless-1 as a novel, Robo1-interacting protein. Treatment with shRNAs reduced levels of Flightless-1 and demonstrated its role in efficient cell-to-cell transfer of HIV-1. These results suggest a novel strategy to limit viral infection in the host by targeting the Slit/Robo pathway with modulation of cytoskeletal elements previously unrecognized in HIV-1 transmission.

Indexed as

Actin-Related Protein 2-3 ComplexActinsCarrier Proteinscdc42 GTP-Binding ProteinCell Surface ExtensionsCytoskeletonDendritic CellsEnzyme ActivationForminsHEK293 CellsHIV-1HIV InfectionsHumansIntercellular Signaling Peptides and ProteinsModels, BiologicalNerve Tissue ProteinsActin-Related Protein 2-3 ComplexActinsCarrier Proteinscdc42 GTP-Binding ProteinDIAPH2 protein, humanFLI1 protein, humanForminsIntercellular Signaling Peptides and ProteinsNerve Tissue ProteinsProto-Oncogene Protein c-fli-1Receptors, ImmunologicRoundabout ProteinsSlit Homolog 2 Proteinsrc-Family KinasesWiskott-Aldrich Syndrome Protein

Identifiers

PMID26582347
PMCPMC4652184
OpenAlexW2202393715

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.