Evidence map›Paper›PMID 11259576›Full record

ArticleMolecular and cellular biology2001

The growth suppressor PML represses transcription by functionally and physically interacting with histone deacetylases.

W S Wu, S Vallian, E Seto, W M Yang, D Edmondson, S Roth, K S Chang

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 152 citations in OpenAlex.

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10 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

W S WuDepartment of Molecular Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
S Vallian
E Seto
W M Yang
D Edmondson
S Roth
K S Chang
The University of Texas MD Anderson Cancer Center · USUniversity of South Florida · US

Funding

MOLECULAR PATHOLOGY OF ACUTE PROMYELOCYTIC LEUKEMIAR01CA055577 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CHANG, KUN-SANG · 1992 to 2012
$2.5M
NCI NIH HHS CA 55577NCI NIH HHS R01 CA055577
6 · The paper itself

Abstract

The growth suppressor promyelocytic leukemia protein (PML) is disrupted by the chromosomal translocation t(15;17) in acute promyelocytic leukemia (APL). PML plays a key role in multiple pathways of apoptosis and regulates cell cycle progression. The present study demonstrates that PML represses transcription by functionally and physically interacting with histone deacetylase (HDAC). Transcriptional repression mediated by PML can be inhibited by trichostatin A, a specific inhibitor of HDAC. PML coimmunoprecipitates a significant level of HDAC activity in several cell lines. PML is associated with HDAC in vivo and directly interacts with HDAC in vitro. The fusion protein PML-RARalpha encoded by the t(15;17) breakpoint interacts with HDAC poorly. PML interacts with all three isoforms of HDAC through specific domains, and its expression deacetylates histone H3 in vivo. Together, the results of our study show that PML modulates histone deacetylation and that loss of this function in APL alters chromatin remodeling and gene expression. This event may contribute to the development of leukemia.

Indexed as

Transcriptional ActivationAnimalsCOS CellsHistone DeacetylasesNeoplasm ProteinsNuclear ProteinsProtein BindingTranscription FactorsTranscription, GeneticTumor Suppressor ProteinsZinc FingersHistone DeacetylasesNeoplasm ProteinsNuclear ProteinsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID11259576
PMCPMC86860
OpenAlexW2126689485

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.