Evidence map›Paper›PMID 16641266›Full record

ArticleJournal of virology2006

NS1 interaction with CKII alpha: novel protein complex mediating parvovirus-induced cytotoxicity.

Jürg P F Nüesch, Jean Rommelaere

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

36 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  15. Article
  16. Poly (I:C) enhances the anti-tumor activity of canine parvovirus NS1 protein by inducing a potent anti-tumor immune response.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  17. Predicting CK2 beta-dependent substrates using linear patterns.Biochemistry and biophysics reports · 2015
    Article
  18. Review
  19. Article
  20. Viral genes as oncolytic agents for cancer therapy.Cellular and molecular life sciences : CMLS · 2015
    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

2 authors at 2 institutions in 1 country.

Jürg P F NüeschProgram Infection and Cancer, Abt. F010 and INSERM U701, Deutsches Krebsforschungszentrum, Heidelberg, Germany. jpf.nuesch@dkfz-heidelberg.de
Jean Rommelaere
DKFZ-ZMBH Alliance · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During a productive infection, the prototype strain of the parvovirus minute virus of mice (MVMp) induces dramatic morphological alterations in permissive A9 fibroblasts, culminating in cell lysis at the end of infection. These cytopathic effects (CPE) result from rearrangements and destruction of the cytoskeletal micro- and intermediate filaments, while other structures such as the nuclear lamina and particularly the microtubule network remain protected throughout the infection (J. P. F. Nüesch et al., Virology 331:159-174, 2005). In order to unravel the mechanism(s) by which parvoviruses trigger CPE, we searched for NS1 interaction partners by differential affinity chromatography, using distinct NS1 mutants debilitated specifically for this function. Thereby, we isolated an NS1 partner polypeptide, whose interaction with NS1 correlated with the competence of the viral product for CPE induction, and further identified it by tandem mass spectrometry and Western blotting analyses to consist of the catalytic subunit of casein kinase II, CKIIalpha. This interaction of NS1 with CKIIalpha suggested interference by the viral protein with intracellular signaling. Using permanent cell lines expressing dominant-negative CKIIalpha mutants, we were able to show that this kinase activity was indeed specifically involved in parvoviral CPE and progeny particle release. Furthermore, the NS1/CKIIalpha complex proved to be able to specifically phosphorylate viral capsids, indicating a mediator function of NS1 for CKII activity and specificity, at least in vitro. Altogether our data suggest that parvovirus-induced CPE is mediated by NS1 interference with intracellular CKII signaling.

Indexed as

Cytotoxicity, ImmunologicAmino Acid SequenceAnimalsBase SequenceCapsid ProteinsCasein Kinase IICytopathogenic Effect, ViralFluorescent Antibody TechniqueHeLa CellsHumansIntracellular FluidMiceMinute Virus of MiceMolecular Sequence DataPhosphorylationSignal TransductionCapsid ProteinsCasein Kinase IINS1 protein, parvovirusViral Nonstructural Proteins

Identifiers

PMID16641266
PMCPMC1472057
OpenAlexW2128197144

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.