Evidence map›Paper›PMID 20230751›Full record

ArticleDevelopmental cell2010

BCL6 canalizes Notch-dependent transcription, excluding Mastermind-like1 from selected target genes during left-right patterning.

Daisuke Sakano, Akiko Kato, Nisarg Parikh, Kelly McKnight, Doris Terry, Branko Stefanovic, Yoichi Kato

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Laterality defects are influenced by timing of treatments and animal model.Differentiation; research in biological diversity · 2012
    Pooled it
  2. Article
  3. Article
  4. Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  8. Mutational profile and EBV strains of extranodal NK/T-cell lymphoma, nasal type in Latin America.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Article
  9. Notch Signaling in B Cell Immune Responses.Frontiers in immunology · 2020
    Review
  10. Article
  11. Article
  12. Epigenetic Reprogramming and Emerging Epigenetic Therapies in CML.Frontiers in cell and developmental biology · 2019
    Review
  13. Allergic TFrontiers in immunology · 2018
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Notch signalling in context.Nature reviews. Molecular cell biology · 2016
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Daisuke SakanoDepartment of Biomedical Sciences, Florida State University, College of Medicine, Tallahassee, FL 32306, USA.
Akiko Kato
Nisarg Parikh
Kelly McKnight
Doris Terry
Branko Stefanovic
Yoichi Kato
Florida State University · US

Funding

The mechanism of Notch signaling pathway in radial glial developmentR03HD052526 · NICHD · FLORIDA STATE UNIVERSITY · PI KATO, YOICHI · 2008 to 2009
$147k
NICHD NIH HHS HD052526NICHD NIH HHS R03 HD052526
6 · The paper itself

Abstract

Although the Notch signaling pathway is one of the most intensely studied intracellular signaling pathways, the mechanisms by which Notch signaling regulates transcription remain incompletely understood. Here, we report that B cell leukemia/lymphoma 6 (BCL6), a transcriptional repressor, is a Notch-associated factor. BCL6 is necessary to maintain the expression of Pitx2 in the left lateral plate mesoderm during the patterning of left-right asymmetry in Xenopus embryos. For this process, BCL6 forms a complex with BCL6 corepressor (BCoR) on the promoters of selected Notch target genes such as enhancer of split related 1. BCL6 also inhibits the transcription of these genes by competing for the Notch1 intracellular domain, preventing the coactivator Mastermind-like1 (MAM1) from binding. These results define a mechanism restricting Notch-activated transcription to cell-type-appropriate subsets of target genes, and elucidate its relevance in vivo during left-right asymmetric development.

Indexed as

AnimalsBase SequenceBody PatterningDNAGene Expression Regulation, DevelopmentalHomeodomain ProteinsIn Vitro TechniquesModels, BiologicalMolecular Sequence DataReceptors, NotchRecombinant Fusion ProteinsRepressor ProteinsRNA InterferenceSignal TransductionTranscription, GeneticXenopusDNAEsr1 protein, XenopusHomeodomain ProteinsMAML1 protein, XenopusReceptors, NotchRecombinant Fusion ProteinsRepressor ProteinsXenopus Proteins

Identifiers

PMID20230751
PMCPMC2841049
OpenAlexW2148839219

What OpenQuestion holds

Textmetadata
LicenceTDM
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.