Evidence map›Paper›PMID 11439334›Full record

ArticleOncogene2001

TEL contacts multiple co-repressors and specifically associates with histone deacetylase-3.

L Wang, S W Hiebert

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 99 citations in OpenAlex.

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  20. NCoR negatively regulates adipogenic differentiation of mesenchymal stem cells.In vitro cellular & developmental biology. Animal · 2015
    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

2 authors at 1 institution in 1 country.

L WangDepartment of Biochemistry and the Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee, TN 37232, USA.
S W Hiebert
Vanderbilt University · US

Funding

TEL AND THE T(12--21) AND B CELL ALLR01CA077274 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 1997 to 2006
$2.1M
SYSTEMATIC STUDY OF BORON RICH ANTIBODY CONJUGATESR01CA068465 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HAWTHORNE, M FREDERICK · 1996 to 1998
–
NCI NIH HHS CA68465NCI NIH HHS R01-CA77274
6 · The paper itself

Abstract

TEL (Translocation-ETS-Leukemia or ETV 6) is disrupted by multiple chromosomal translocations in acute leukemia. The loss of heterozygosity at the TEL locus in leukemias and the hemizygous deletion of TEL that is observed in various tumors, suggests that TEL is a tumor suppressor. Overexpression of TEL alters cellular morphology and represses the expression of the matrix metalloproteinase stromelysin-1. Based on these studies, deletion analysis was used to define the minimal repression domains of TEL. TEL-mediated repression required both the N-terminal pointed domain and a central region composed of amino acids 268-303. The mSin3A and N-CoR corepressors bind to the pointed domain and the central repression domain of TEL, respectively. Unexpectedly, histone deacetylase-3, but not other histone deacetylases, also associates with the central region of TEL. Histone deacetylase-3 interacts with a TEL mutant that cannot bind N-CoR, suggesting that this is a direct interaction with TEL. In addition, histone H3 was under-acetylated near the TEL-binding sites in the endogenous stromelysin-1 promoter when TEL was expressed. Furthermore, trichostatin A, a potent histone deacetylase inhibitor, impaired TEL-dependent repression of the stromelysin-1 promoter. Finally, while TEL-expression induced cellular aggregation of Ras-transformed cells, Trichostatin A reversed the TEL-induced cellular aggregation phenotype. Thus, the cumulative data suggests that histone deacetylase-3 activity is required for the transcriptional functions of TEL.

Indexed as

Genes, Tumor Suppressor3T3 CellsAcetylationAnimalsBinding SitesChlorocebus aethiopsChromosome MappingCOS CellsDNA-Binding ProteinsETS Translocation Variant 6 ProteinHistone Deacetylase 3Histone DeacetylasesHistonesMatrix Metalloproteinase 3MiceMutagenesisDNA-Binding ProteinsETS Translocation Variant 6 ProteinHistone Deacetylase 3Histone DeacetylasesHistonesMatrix Metalloproteinase 3Ncor1 protein, mouseNuclear ProteinsNuclear Receptor Co-Repressor 1Proto-Oncogene Proteins c-etsRepressor ProteinsSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexTranscription Factors

Identifiers

PMID11439334
OpenAlexW2318731296

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.