Evidence map›Paper›PMID 19211936›Full record

ArticleBlood2009

Mef2C is a lineage-restricted target of Scl/Tal1 and regulates megakaryopoiesis and B-cell homeostasis.

Christos Gekas, Katrin E Rhodes, Laurraine M Gereige, Hildur Helgadottir, Roberto Ferrari, Siavash K Kurdistani, Encarnación Montecino-Rodriguez, Rhonda Bassel-Duby, Eric Olson, Andrei V Krivtsov and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Molecular and Biological Function of MEF2D in Leukemia.Advances in experimental medicine and biology · 2024
    Review
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  10. Article
  11. Article
  12. Review
  13. Article
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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

14 authors at 5 institutions in 1 country.

Christos GekasDepartment of Molecular, Cell and Developmental Biology, University of California-Los Angeles, Los Angeles, CA 90095, USA.
Katrin E Rhodes
Laurraine M Gereige
Hildur Helgadottir
Roberto Ferrari
Siavash K Kurdistani
Encarnación Montecino-Rodriguez
Rhonda Bassel-Duby
Eric Olson
Andrei V Krivtsov
Scott Armstrong
Stuart H Orkin
Matteo Pellegrini
Hanna K A Mikkola
University of California, Los Angeles · USHarvard University · USThe University of Texas Southwestern Medical Center · USDana-Farber Cancer Institute · USUCLA Jonsson Comprehensive Cancer Center

Funding

UCLA NIGMS T32 Program AssessmentT32GM007185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TORRES, JORGE · 1985 to 2020
$21.7M
NIGMS NIH HHS GM07185NIGMS NIH HHS T32 GM007185
6 · The paper itself

Abstract

The basic helix-loop-helix transcription factor stem cell leukemia gene (Scl) is a master regulator for hematopoiesis essential for hematopoietic specification and proper differentiation of the erythroid and megakaryocyte lineages. However, the critical downstream targets of Scl remain undefined. Here, we identified a novel Scl target gene, transcription factor myocyte enhancer factor 2 C (Mef2C) from Scl(fl/fl) fetal liver progenitor cell lines. Analysis of Mef2C(-/-) embryos showed that Mef2C, in contrast to Scl, is not essential for specification into primitive or definitive hematopoietic lineages. However, adult VavCre(+)Mef2C(fl/fl) mice exhibited platelet defects similar to those observed in Scl-deficient mice. The platelet counts were reduced, whereas platelet size was increased and the platelet shape and granularity were altered. Furthermore, megakaryopoiesis was severely impaired in vitro. Chromatin immunoprecipitation microarray hybridization analysis revealed that Mef2C is directly regulated by Scl in megakaryocytic cells, but not in erythroid cells. In addition, an Scl-independent requirement for Mef2C in B-lymphoid homeostasis was observed in Mef2C-deficient mice, characterized as severe age-dependent reduction of specific B-cell progenitor populations reminiscent of premature aging. In summary, this work identifies Mef2C as an integral member of hematopoietic transcription factors with distinct upstream regulatory mechanisms and functional requirements in megakaryocyte and B-lymphoid lineages.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBlood PlateletsB-LymphocytesCell LineageCell Line, TransformedFemaleGene Expression Regulation, DevelopmentalHematopoietic Stem CellsHomeostasisLiverLymphopoiesisMaleMEF2 Transcription FactorsMegakaryocytesMiceBasic Helix-Loop-Helix ProteinsMef2c protein, mouseMEF2 Transcription FactorsMyogenic Regulatory FactorsProto-Oncogene ProteinsTal1 protein, mouseT-Cell Acute Lymphocytic Leukemia Protein 1

Identifiers

PMID19211936
PMCPMC2945827
OpenAlexW2046790140

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.