Evidence map›Paper›PMID 24742922›Full record

ArticleOncotarget2014

Inhibition of protein kinase II (CK2) prevents induced signal transducer and activator of transcription (STAT) 1/3 and constitutive STAT3 activation.

Samadhi Aparicio-Siegmund, Jan Sommer, Niloufar Monhasery, Ralf Schwanbeck, Eric Keil, David Finkenstädt, Klaus Pfeffer, Stefan Rose-John, Jürgen Scheller, Christoph Garbers

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Regulation of cancer progression by CK2: an emerging therapeutic target.Medical oncology (Northwood, London, England) · 2024
    Review
  4. Article
  5. Review
  6. Review
  7. Leukemia inhibitory factor, a double-edged sword with therapeutic implications in human diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. CK2 Phosphorylating IFrontiers in molecular neuroscience · 2018
    Article
  17. Article
  18. Article
  19. Review
  20. 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

10 authors at 2 institutions in 1 country.

Samadhi Aparicio-SiegmundInstitute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany;
Jan Sommer
Niloufar Monhasery
Ralf Schwanbeck
Eric Keil
David Finkenstädt
Klaus Pfeffer
Stefan Rose-John
Jürgen Scheller
Christoph Garbers
Heinrich Heine University Düsseldorf · DEKiel University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Janus kinase / signal transducer and activator of transcription (Jak/STAT) pathway can be activated by many different cytokines, among them all members of the Interleukin (IL-)6 family. Dysregulation of this pathway, resulting in its constitutive activation, is associated with chronic inflammation and cancer development. In the present study, we show that activity of protein kinase II (CK2), a ubiquitously expressed serine/threonine kinase, is needed for induced activation of STAT1 and STAT3 by IL-6 classic and trans-signaling, IL-11, IL-27, oncostatin M (OSM), leukemia inhibitory factor (LIF) and cardiotrophin-1 (CT-1). Inhibition of CK2 efficiently prevented STAT phosphorylation and inhibited cytokine-dependent cell proliferation in a Jak1-dependent manner. Conversely, forced activation of CK2 alone was not sufficient to induce activation of the Jak/STAT signaling pathway. Inhibition of CK2 in turn inhibited Jak1-dependent STAT activation by oncogenic gp130 mutations. Furthermore, CK2 inhibition diminished the Jak1- and Src kinase-dependent phosphorylation of a constitutively active STAT3 mutant recently described in human large granular lymphocytic leukemia. In conclusion, we characterize CK2 as an essential component of the Jak/STAT pathway. Pharmacologic inhibition of this kinase is therefore a promising strategy to treat human inflammatory diseases and malignancies associated with constitutive activation of the Jak/STAT pathway.

Indexed as

AnimalsBlotting, WesternCasein Kinase IICell Line, TumorEnzyme ActivationHumansJanus KinasesMiceSignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorTransfectionCasein Kinase IIJanus KinasesSTAT1 protein, humanSTAT1 Transcription FactorSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID24742922
PMCPMC4039151
OpenAlexW1897588476

What OpenQuestion holds

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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.