Evidence map›Paper›PMID 15516979›Full record

ArticleOncogene2004

The serine-threonine kinase MNK1 is post-translationally stabilized by PML-RARalpha and regulates differentiation of hematopoietic cells.

Jennifer Worch, Lara Tickenbrock, Joachim Schwäble, Björn Steffen, Thomas Cauvet, Barbara Mlody, Horst Buerger, H Phillip Koeffler, Wolfgang E Berdel, Hubert Serve and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Mnk kinase pathway: Cellular functions and biological outcomes.World journal of biological chemistry · 2014
    Review
  8. Article
  9. Article
  10. Article
  11. Regulation of mRNA translation by signaling pathways.Cold Spring Harbor perspectives in biology · 2012
    Review
  12. Review
  13. Combined deficiency for MAP kinase-interacting kinase 1 and 2 (Mnk1 and Mnk2) delays tumor development.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  14. Article
  15. Article
  16. 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

11 authors at 2 institutions in 2 countries.

Jennifer WorchDepartment of Medicine, Hematology and Oncology, University of Münster, Domagkstr. 3, 48129 Münster, Germany.
Lara Tickenbrock
Joachim Schwäble
Björn Steffen
Thomas Cauvet
Barbara Mlody
Horst Buerger
H Phillip Koeffler
Wolfgang E Berdel
Hubert Serve
Carsten Müller-Tidow
University of Münster · DECedars-Sinai Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microarray analyses were performed to identify target genes that are shared by the acute myeloid leukemia (AML) translocation products PML-RARalpha, PLZF-RARalpha and AML1-ETO in inducibly transfected U937 cell lines. The cytoplasmic serine and threonine kinase MNK1 was identified as one of the target genes. At the protein level, MNK1 was significantly induced by each of the three fusion proteins. Protein half-life analyses showed that PML-RARalpha enhanced MNK1 protein stability in U937 cells and ATRA exposure decreased MNK1 half-life in NB4 cells. EIF4E, the main MNK1 substrate, plays a role in the pathogenesis of a variety of cancers. Upon MNK1 overexpression, eIF4E phosphorylation increased as a sign of functional activation. Interestingly, MNK1 protein expression decreased during myeloid differentiation. Inhibition of MNK1 activity by a specific inhibitor (CGP57380) enhanced differentiation of HL60 and 32D cells, further suggesting a role for MNK1 in the myeloid differentiation. In addition, kinase dead mutants of MNK1 significantly impaired proliferation of 32D cells. Immunohistochemistry of primary AML bone marrow biopsies showed strong cytoplasmic MNK1 expression in 25 of 99 AML specimens (25%). MNK1 expression was associated with high levels of c-myc expression. Taken together, we identified MNK1 as a target gene of several leukemogenic fusion proteins in AML. MNK1 plays a role in myeloid differentiation. These data suggest a role for MNK1 in the AML fusion protein-associated differentiation block.

Indexed as

Base SequenceBone Marrow CellsCell DifferentiationCell Line, TumorDNA PrimersEukaryotic Initiation Factor-4EHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsOncogene Proteins, FusionPhosphorylationProtein Processing, Post-TranslationalProtein Serine-Threonine KinasesRNA, MessengerDNA PrimersEukaryotic Initiation Factor-4EIntracellular Signaling Peptides and ProteinsMKNK1 protein, humanNeoplasm ProteinsOncogene Proteins, Fusionpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinProtein Serine-Threonine KinasesRNA, Messenger

Identifiers

PMID15516979
OpenAlexW1999201187

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.