Evidence map›Paper›PMID 26900922›Full record

ArticlePLoS genetics2016

MEF2C and EBF1 Co-regulate B Cell-Specific Transcription.

Nikki R Kong, Matthew Davis, Li Chai, Astar Winoto, Robert Tjian

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. EBF1 is continuously required for stabilizing local chromatin accessibility in pro-B cells.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. IPiScience · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Nikki R KongDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, United States of America.
Matthew DavisDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, United States of America.
Li ChaiDepartment of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, United States of America.
Astar WinotoDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, United States of America.
Robert TjianDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, United States of America.
University of California, Berkeley · USBrigham and Women's Hospital · US

Funding

TRANSFUSION BIOLOGY AND MEDICINET32HL066987 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI JOHN P MANIS · 2001 to 2026
$10.2M
Howard Hughes Medical InstituteNHLBI NIH HHS T32 HL066987
6 · The paper itself

Abstract

Hematopoietic stem cells are capable of self-renewal or differentiation along three main lineages: myeloid, erythroid, and lymphoid. One of the earliest lineage decisions for blood progenitor cells is whether to adopt the lymphoid or myeloid fate. Previous work had shown that myocyte enhancer factor 2C (MEF2C) is indispensable for the lymphoid fate decision, yet the specific mechanism of action remained unclear. Here, we have identified early B cell factor-1 (EBF1) as a co-regulator of gene expression with MEF2C. A genome-wide survey of MEF2C and EBF1 binding sites identified a subset of B cell-specific genes that they target. We also determined that the p38 MAPK pathway activates MEF2C to drive B cell differentiation. Mef2c knockout mice showed reduced B lymphoid-specific gene expression as well as increased myeloid gene expression, consistent with MEF2C's role as a lineage fate regulator. This is further supported by interaction between MEF2C and the histone deacetylase, HDAC7, revealing a likely mechanism to repress the myeloid transcription program. This study thus elucidates both activation and repression mechanisms, identifies regulatory partners, and downstream targets by which MEF2C regulates lymphoid-specific differentiation.

Indexed as

Transcription, GeneticB-LymphocytesCell DifferentiationCell LineCell LineageHematopoietic Stem CellsHistone DeacetylasesHumansImmunoprecipitationMEF2 Transcription FactorsMyeloid Cellsp38 Mitogen-Activated Protein KinasesPhosphorylationPrecursor Cells, B-LymphoidProtein TransportSubcellular FractionsEBF1 protein, humanHistone DeacetylasesMEF2 Transcription Factorsp38 Mitogen-Activated Protein KinasesTrans-Activators

Identifiers

PMID26900922
PMCPMC4762780
OpenAlexW2286525704

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.