Evidence map›Paper›PMID 23911289›Full record

ArticleCell reports2013

A hybrid mechanism of action for BCL6 in B cells defined by formation of functionally distinct complexes at enhancers and promoters.

Katerina Hatzi, Yanwen Jiang, Chuanxin Huang, Francine Garrett-Bakelman, Micah D Gearhart, Eugenia G Giannopoulou, Paul Zumbo, Kevin Kirouac, Srividya Bhaskara, Jose M Polo and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing 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

122 citing papers in PubMed, 193 citations in OpenAlex.

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  16. The N-Terminal Part ofInternational journal of molecular sciences · 2023
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62 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

20 authors at 6 institutions in 3 countries.

Katerina HatziDivision of Hematology and Medical Oncology, Weill Cornell Medical College, Cornell University, New York, NY 10065, USA.
Yanwen Jiang
Chuanxin Huang
Francine Garrett-Bakelman
Micah D Gearhart
Eugenia G Giannopoulou
Paul Zumbo
Kevin Kirouac
Srividya Bhaskara
Jose M Polo
Matthias Kormaksson
Alexander D MacKerell
Fengtian Xue
Christopher E Mason
Scott W Hiebert
Gilbert G Prive
Leandro Cerchietti
Vivian J Bardwell
Olivier Elemento
Ari Melnick
Cornell University · USMasonic Cancer CenterOntario Institute for Cancer Research · CAUniversity of Maryland, Baltimore · USVanderbilt University · USAustralian Regenerative Medicine Institute · AU

Funding

Hdac3 as a therapeutic target in BCL6-dependent lymphomaR01CA164605 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 2012 to 2022
$3.9M
Molecular Basis of Action of the Putative Oncogene BCL6R01CA071540 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BARDWELL, VIVIAN J · 2002 to 2012
$3.0M
Molecular Targeting of Diffuse Large B-cell LymphomaR01CA143032 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MELNICK, ARI M. · 2010 to 2014
$2.8M
Transcriptional silencing by the BCL6 oncoproteinR01CA104348 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MELNICK, ARI M. · 2004 to 2014
$2.6M
NCI NIH HHS R01 CA071540NCI NIH HHS R01 CA104348NCI NIH HHS R01 CA143032NCI NIH HHS R01 CA164605
6 · The paper itself

Abstract

The BCL6 transcriptional repressor is required for the development of germinal center (GC) B cells and diffuse large B cell lymphomas (DLBCLs). Although BCL6 can recruit multiple corepressors, its transcriptional repression mechanism of action in normal and malignant B cells is unknown. We find that in B cells, BCL6 mostly functions through two independent mechanisms that are collectively essential to GC formation and DLBCL, both mediated through its N-terminal BTB domain. These are (1) the formation of a unique ternary BCOR-SMRT complex at promoters, with each corepressor binding to symmetrical sites on BCL6 homodimers linked to specific epigenetic chromatin features, and (2) the "toggling" of active enhancers to a poised but not erased conformation through SMRT-dependent H3K27 deacetylation, which is mediated by HDAC3 and opposed by p300 histone acetyltransferase. Dynamic toggling of enhancers provides a basis for B cells to undergo rapid transcriptional and phenotypic changes in response to signaling or environmental cues.

Indexed as

AnimalsB-LymphocytesCell Line, TumorDNA-Binding ProteinsHeterograftsHumansLymphoma, Large B-Cell, DiffuseMiceModels, MolecularPromoter Regions, GeneticProto-Oncogene Proteins c-bcl-6Signal TransductionBCL6 protein, humanBcl6 protein, mouseDNA-Binding ProteinsProto-Oncogene Proteins c-bcl-6

Identifiers

PMID23911289
PMCPMC3854650
OpenAlexW2007861438

What OpenQuestion holds

Textmetadata
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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.