Evidence map›Paper›PMID 17182689›Full record

ArticleJournal of virology2007

In vitro treatment of human monocytes/macrophages with myristoylated recombinant Nef of human immunodeficiency virus type 1 leads to the activation of mitogen-activated protein kinases, IkappaB kinases, and interferon regulatory factor 3 and to the release of beta interferon.

Giorgio Mangino, Zulema A Percario, Gianna Fiorucci, Gabriele Vaccari, Santiago Manrique, Giovanna Romeo, Maurizio Federico, Matthias Geyer, Elisabetta Affabris

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Inhibition of apoptosis signal-regulating kinase 1 mitigates the pathogenesis of human immunodeficiency virus-associated nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021
    Article
  4. Review
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  6. Review
  7. Article
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  13. Article
  14. The macrophage: a therapeutic target in HIV-1 infection.Molecular and cellular therapies · 2014
    Review
  15. Review
  16. PAK in pathogen-host interactions.Cellular logistics · 2012
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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

9 authors at 5 institutions in 2 countries.

Giorgio ManginoDepartment of Biology-University Roma Tre, Viale G. Marconi 446, 00146 Rome, Italy.
Zulema A Percario
Gianna Fiorucci
Gabriele Vaccari
Santiago Manrique
Giovanna Romeo
Maurizio Federico
Matthias Geyer
Elisabetta Affabris
Roma Tre University · ITIstituto Superiore di Sanità · ITInstitute of Molecular Biology and Pathology · ITMax Planck Institute of Molecular Physiology · DESapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The viral protein Nef is a virulence factor that plays multiple roles during the early and late phases of human immunodeficiency virus (HIV) replication. Nef regulates the cell surface expression of critical proteins (including down-regulation of CD4 and major histocompatibility complex class I), T-cell receptor signaling, and apoptosis, inducing proapoptotic effects in uninfected bystander cells and antiapoptotic effects in infected cells. It has been proposed that Nef intersects the CD40 ligand signaling pathway in macrophages, leading to modification in the pattern of secreted factors that appear able to recruit and activate T lymphocytes, rendering them susceptible to HIV infection. There is also increasing evidence that in vitro cell treatment with Nef induces signaling effects. Exogenous Nef treatment is able to induce apoptosis in uninfected T cells, maturation in dendritic cells, and suppression of CD40-dependent immunoglobulin class switching in B cells. Previously, we reported that Nef treatment of primary human monocyte-derived macrophages (MDMs) induces a cycloheximide-independent activation of NF-kappaB and the synthesis and secretion of a set of chemokines/cytokines that activate STAT1 and STAT3. Here, we show that Nef treatment is capable of hijacking cellular signaling pathways, inducing a very rapid regulatory response in MDMs that is characterized by the rapid and transient phosphorylation of the alpha and beta subunits of the IkappaB kinase complex and of JNK, ERK1/2, and p38 mitogen-activated protein kinase family members. In addition, we have observed the activation of interferon regulatory factor 3, leading to the synthesis of beta interferon mRNA and protein, which in turn induces STAT2 phosphorylation. All of these effects require Nef myristoylation.

Indexed as

Enzyme ActivationGene Products, nefHIV-1HumansI-kappa B KinaseInterferon-betaInterferon Regulatory Factor-3In Vitro TechniquesMitogen-Activated Protein KinasesModels, BiologicalMonocytesMyristic Acidnef Gene Products, Human Immunodeficiency VirusRecombinant Fusion ProteinsGene Products, nefI-kappa B KinaseInterferon-betaInterferon Regulatory Factor-3Mitogen-Activated Protein KinasesMyristic Acidnef Gene Products, Human Immunodeficiency VirusRecombinant Fusion Proteins

Identifiers

PMID17182689
PMCPMC1865981
OpenAlexW2095056958

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.