Evidence map›Paper›PMID 10637511›Full record

ArticleOncogene1999

The N-terminal domain of human TAFII68 displays transactivation and oncogenic properties.

A Bertolotti, B Bell, L Tora

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

35 citing papers in PubMed, 86 citations in OpenAlex.

  1. Causal ALS genes impact the MHC class II antigen presentation pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  4. Distinct roles of hnRNPH1 low-complexity domains in splicing and transcription.Proceedings of the National Academy of Sciences of the United States of America · 2021
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  5. Fused in sarcoma regulates DNA replication timing and kinetics.The Journal of biological chemistry · 2021
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  6. Diagnostics (Basel, Switzerland) · 2021
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  7. Redox-mediated regulation of low complexity domain self-association.Current opinion in genetics & development · 2021
    Review
  8. Molecular therapy. Nucleic acids · 2021
    Article
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  19. Article
  20. Fus expression patterns in developing tooth.Development & reproduction · 2013
    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

3 authors at 2 institutions in 1 country.

A BertolottiInstitut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, BP 163 - 67404 Illkirch Cedex, CU de Strasbourg, France.
B Bell
L Tora
Institut de génétique et de biologie moléculaire et cellulaire · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Ewing tumor, the (11;22) chromosomal translocation produces a chimeric molecule composed of the amino-terminal domain of EWS fused to the carboxyl-terminal DNA-binding domain of FLI-1. Previously, we have identified a novel protein TAFII68, which is highly similar to EWS and another closely related protein TLS (also called FUS). We demonstrate that the N-terminus of TAFII68 efficiently stimulates transcription when fused to two different DNA binding domains and that overexpression of TAFII68-FLI-1 chimeras in NIH3T3 cells leads to oncogenic transformation. We have also investigated the molecular mechanisms which could account for the transcriptional activation and the oncogenic transformation potential of the N-termini of TAFII68 and EWS. Thus, we have tested whether the artificial recruitment of components of the preinitiation complex (PIC) or a histone acetyltransferase (HAT) could bypass the requirement for the activation domains of either EWS or TAFII68. Recruitment of individual components of the transcription machinery or the GCN5 HAT is not sufficient to promote activation from FLI-1 responsive genes either in transfection experiments or in oncogenic transformation assays. These results suggest that the TAFII68 or EWS activation domains enhance a step after PIC formation in the transcriptional activation process.

Indexed as

Cell Transformation, NeoplasticProto-Oncogene ProteinsTATA-Binding Protein Associated Factors3T3 CellsAnimalsBone NeoplasmsChromosomes, Human, Pair 11Chromosomes, Human, Pair 22DNA-Binding ProteinsGenes, ReporterHeLa CellsHumansMiceProto-Oncogene Protein c-fli-1Recombinant Fusion ProteinsSarcoma, EwingDNA-Binding ProteinsFli1 protein, mouseProto-Oncogene Protein c-fli-1Proto-Oncogene ProteinsRecombinant Fusion ProteinsTAF15 protein, humanTATA-Binding Protein Associated FactorsTrans-ActivatorsTranscription Factors

Identifiers

PMID10637511
OpenAlexW2316715032

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.