Evidence map›Paper›PMID 9687511›Full record

ArticleThe EMBO journal1998

TLS/FUS, a pro-oncogene involved in multiple chromosomal translocations, is a novel regulator of BCR/ABL-mediated leukemogenesis.

D Perrotti, S Bonatti, R Trotta, R Martinez, T Skorski, P Salomoni, E Grassilli, R V Lozzo, D R Cooper, B Calabretta

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.2field-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

57 citing papers in PubMed, 129 citations in OpenAlex.

  1. Article
  2. Article
  3. MiRNA-142-3P and FUS can be Sponged by Long Noncoding RNAFrontiers in molecular biosciences · 2021
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. 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 1 institution in 1 country.

D PerrottiDepartment of Microbiology and Immunology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA. perrott1@jeflin.tjn.edu
S Bonatti
R Trotta
R Martinez
T Skorski
P Salomoni
E Grassilli
R V Lozzo
D R Cooper
B Calabretta
Jefferson College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The leukemogenic potential of BCR/ABL oncoproteins depends on their tyrosine kinase activity and involves the activation of several downstream effectors, some of which are essential for cell transformation. Using electrophoretic mobility shift assays and Southwestern blot analyses with a double-stranded oligonucleotide containing a zinc finger consensus sequence, we identified a 68 kDa DNA-binding protein specifically induced by BCR/ABL. The peptide sequence of the affinity-purified protein was identical to that of the RNA-binding protein FUS (also called TLS). Binding activity of FUS required a functional BCR/ABL tyrosine kinase necessary to induce PKCbetaII-dependent FUS phosphorylation. Moreover, suppression of PKCbetaII activity in BCR/ABL-expressing cells by treatment with the PKCbetaII inhibitor CGP53353, or by expression of a dominant-negative PKCbetaII, markedly impaired the ability of FUS to bind DNA. Suppression of FUS expression in myeloid precursor 32Dcl3 cells transfected with a FUS antisense construct was associated with upregulation of the granulocyte-colony stimulating factor receptor (G-CSFR) and downregulation of interleukin-3 receptor (IL-3R) beta-chain expression, and accelerated G-CSF-stimulated differentiation. Downregulation of FUS expression in BCR/ABL-expressing 32Dcl3 cells was associated with suppression of growth factor-independent colony formation, restoration of G-CSF-induced granulocytic differentiation and reduced tumorigenic potential in vivo. Together, these results suggest that FUS might function as a regulator of BCR/ABL leukemogenesis, promoting growth factor independence and preventing differentiation via modulation of cytokine receptor expression.

Indexed as

Translocation, GeneticAmino Acid SequenceAnimalsCell DifferentiationCell DivisionDNA-Binding ProteinsFusion Proteins, bcr-ablGene Expression Regulation, NeoplasticGrowth SubstancesHematopoietic Stem CellsHeterogeneous-Nuclear RibonucleoproteinsHumansLeukemia, MyeloidMiceMice, Inbred ICRMice, SCIDDNA-Binding ProteinsFusion Proteins, bcr-ablGrowth SubstancesHeterogeneous-Nuclear RibonucleoproteinsProtein Kinase CProtein-Tyrosine KinasesRibonucleoproteinsRNA-Binding Protein FUS

Identifiers

PMID9687511
PMCPMC1170776
OpenAlexW2164627733

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.