Evidence map›Paper›PMID 18710951›Full record

ArticleMolecular and cellular biology2008

OTT-MAL is a deregulated activator of serum response factor-dependent gene expression.

Arnaud Descot, Monika Rex-Haffner, Geneviève Courtois, Dominique Bluteau, Antje Menssen, Thomas Mercher, Olivier A Bernard, Richard Treisman, Guido Posern

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. NNature reviews. Cancer · 2026
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  6. MRTF: Basic Biology and Role in Kidney Disease.International journal of molecular sciences · 2021
    Review
  7. Acute Megakaryocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2020
    Review
  8. Review
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  10. Article
  11. Review
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  14. Normal and malignant megakaryopoiesis.Expert reviews in molecular medicine · 2011
    Review
  15. Mouse models of diseases of megakaryocyte and platelet homeostasis.Mammalian genome : official journal of the International Mammalian Genome Society · 2011
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

9 authors at 4 institutions in 3 countries.

Arnaud DescotMax Planck Institute of Biochemistry, Department of Molecular Biology, Martinsried, Germany.
Monika Rex-Haffner
Geneviève Courtois
Dominique Bluteau
Antje Menssen
Thomas Mercher
Olivier A Bernard
Richard Treisman
Guido Posern
Max Planck Institute of Biochemistry · DEHôpital Necker-Enfants Malades · FRInserm · FRCancer Research UK · GB

Funding

Cancer Research UK
6 · The paper itself

Abstract

The OTT-MAL/RBM15-MKL1 fusion protein is the result of the recurrent translocation t(1;22) in acute megakaryocytic leukemia in infants. How it contributes to the malignancy is unknown. The 3' fusion partner, MAL/MKL1/MRTF-A, is a transcriptional coactivator of serum response factor (SRF). MAL plays a key role in regulated gene expression depending on Rho family GTPases and G-actin. Here we demonstrate that OTT-MAL is a constitutive activator of SRF and target gene expression. This requires the SRF-binding motif and the MAL-derived transactivation domain. OTT-MAL localizes to the nucleus and is not regulated by upstream signaling. OTT-MAL deregulation reflects its independence from control by G-actin, which fails to interact with OTT-MAL in coimmunoprecipitation experiments. Regulation cannot be restored by reintroduction of the entire MAL N terminus into the fusion protein. OTT-MAL also caused a delayed induction of the MAL-independent, ternary complex factor-dependent target genes c-fos and egr-1 and the mitogen-activated protein kinase/Erk pathway. With testing in heterologous tissue culture systems, however, we observed considerable antiproliferative effects of OTT-MAL. Our data suggest that the deregulated activation of MAL-dependent and -independent promoters results in tissue-specific functions of OTT-MAL.

Indexed as

Gene Expression RegulationActinsAnimalsEarly Growth Response Protein 1Extracellular Signal-Regulated MAP KinasesHeLa CellsHumansIntracellular SpaceMiceNIH 3T3 CellsOncogene Proteins, FusionPhosphorylationProtein BindingProtein Structure, TertiaryProtein TransportProto-Oncogene Proteins c-fosActinsEarly Growth Response Protein 1Extracellular Signal-Regulated MAP KinasesOncogene Proteins, FusionOTT-MAL fusion protein, humanProto-Oncogene Proteins c-fosrhoA GTP-Binding ProteinSerum Response FactorTernary Complex Factors

Identifiers

PMID18710951
PMCPMC2577437
OpenAlexW2137750008

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.