Evidence map›Paper›PMID 19062179›Full record

ArticleGlia2009

Glial cell type-specific subcellular localization of 14-3-3 zeta: an implication for JCV tropism.

Shivani Lamba, Veerasamy Ravichandran, Eugene O Major

Abstract read
In one paragraph

Article in Glia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Targeting 14-3-3zeta in cancer therapy.Cancer gene therapy · 2012
    Review
  9. Article
  10. Methamphetamine and HIV-1 Tat down regulate β-catenin signaling: implications for methampetamine abuse and HIV-1 co-morbidity.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011
    Article
  11. 14-3-3 proteins as potential therapeutic targets.Seminars in cell & developmental biology · 2011
    Review
  12. 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

3 authors at 2 institutions in 1 country.

Shivani LambaLaboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1296, USA.
Veerasamy Ravichandran
Eugene O Major
National Institute of Neurological Disorders and Stroke · USNational Institutes of Health · US

Funding

Lineage pathway differentiation of CNS progenitor cellsZIANS003048 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI NATH, AVINDRA · 2009 to 2015
$2.8M
Lineage pathway differentiation of CNS progenitor cellsZ01NS003048 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI MAJOR, EUGENE O. · 2007 to 2008
$1.5M
Intramural NIH HHS Z01 NS003048
6 · The paper itself

Abstract

14-3-3 Isoforms are shown to be upregulated or accumulated in the glial cells of autopsied patient brains affected with progressive multifocal leukoencephalopathy (PML), a demylinating disease caused by JC virus (JCV). The possible involvement of 14-3-3 in JCV tropism, however, has never been examined. To investigate a potential relationship between 14-3-3 isoforms and JCV in vitro, we examined the localization of six 14-3-3 isoforms in human neural progenitors and progenitor-derived astrocytes (PDAs) in cells without JCV exposure. The 14-3-3 zeta isoform was initially localized in the progenitor cytoplasm. When differentiation of progenitors into PDAs was induced, the zeta isoform was translocated into the nucleus. However, upon JCV infection, progenitor cells exhibited an uncharacteristic 14-3-3 zeta nuclear presence in the few cells that became infected. JCV-treated PDAs showed elevated levels of 14-3-3 zeta compared with noninfected PDAs. Treatment with TGF-beta1, a known stimulant of JCV multiplication, increased the overall number of infected cells and the otherwise absent nuclear presence of 14-3-3 zeta in progenitors. These results suggest that the nuclear presence of 14-3-3 zeta may play a role in JCV infection, and that the isoform may in part determine JCV susceptibility in these cell types.

Indexed as

14-3-3 ProteinsActive Transport, Cell NucleusAstrocytesBlotting, WesternCell NucleusCells, CulturedFluorescent Antibody TechniqueHumansImmunoassayJC VirusNeuronsStem CellsTransforming Growth Factor beta114-3-3 ProteinsTransforming Growth Factor beta1

Identifiers

PMID19062179
PMCPMC4605217
OpenAlexW2093187449

What OpenQuestion holds

Textmetadata
LicenceTDM
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.