Evidence map›Paper›PMID 32019925›Full record

ArticleNature communications2020

A central role of IKK2 and TPL2 in JNK activation and viral B-cell transformation.

Stefanie Voigt, Kai R Sterz, Fabian Giehler, Anne-Wiebe Mohr, Joanna B Wilson, Andreas Moosmann, Arnd Kieser

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

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  16. Signaling pathways of EBV-induced oncogenesis.Cancer cell international · 2021
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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

7 authors at 3 institutions in 2 countries.

Stefanie VoigtHelmholtz Centre Munich - German Research Centre for Environmental Health, Research Unit Gene Vectors, Marchioninistrasse 25, 81377, Munich, Germany.
Kai R SterzHelmholtz Centre Munich - German Research Centre for Environmental Health, Research Unit Gene Vectors, Marchioninistrasse 25, 81377, Munich, Germany.ORCID http://orcid.org/0000-0002-7225-0485
Fabian GiehlerHelmholtz Centre Munich - German Research Centre for Environmental Health, Research Unit Gene Vectors, Marchioninistrasse 25, 81377, Munich, Germany.
Anne-Wiebe MohrHelmholtz Centre Munich - German Research Centre for Environmental Health, Research Unit Gene Vectors, Marchioninistrasse 25, 81377, Munich, Germany.ORCID http://orcid.org/0000-0002-5544-4595
Joanna B WilsonSchool of Life Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ, UK.ORCID http://orcid.org/0000-0003-4715-2530
Andreas MoosmannHelmholtz Centre Munich - German Research Centre for Environmental Health, Research Unit Gene Vectors, Marchioninistrasse 25, 81377, Munich, Germany.ORCID http://orcid.org/0000-0001-8044-5146
Arnd KieserHelmholtz Centre Munich - German Research Centre for Environmental Health, Research Unit Gene Vectors, Marchioninistrasse 25, 81377, Munich, Germany. a.kieser@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0003-0783-1950
Helmholtz Zentrum München · DEHelmholtz Association of German Research Centres · DEUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IκB kinase 2 (IKK2) is well known for its pivotal role as a mediator of the canonical NF-κB pathway, which has important functions in inflammation and immunity, but also in cancer. Here we identify a novel and critical function of IKK2 and its co-factor NEMO in the activation of oncogenic c-Jun N-terminal kinase (JNK) signaling, induced by the latent membrane protein 1 (LMP1) of Epstein-Barr virus (EBV). Independent of its kinase activity, the TGFβ-activated kinase 1 (TAK1) mediates LMP1 signaling complex formation, NEMO ubiquitination and subsequent IKK2 activation. The tumor progression locus 2 (TPL2) kinase is induced by LMP1 via IKK2 and transmits JNK activation signals downstream of IKK2. The IKK2-TPL2-JNK axis is specific for LMP1 and differs from TNFα, Interleukin-1 and CD40 signaling. This pathway mediates essential LMP1 survival signals in EBV-transformed human B cells and post-transplant lymphoma, and thus qualifies as a target for treatment of EBV-induced cancer.

Indexed as

AnimalsB-LymphocytesCell Line, TumorCell Transformation, ViralHerpesvirus 4, HumanHumansI-kappa B KinaseLymphomaMAP Kinase Kinase 4MAP Kinase Kinase KinasesMiceProto-Oncogene ProteinsSignal TransductionI-kappa B KinaseIKBKB protein, humanMAP3K8 protein, humanMAP Kinase Kinase 4MAP Kinase Kinase KinasesProto-Oncogene Proteins

Identifiers

PMID32019925
PMCPMC7000802
OpenAlexW3005286127

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.