Evidence map›Paper›PMID 21695229›Full record

ArticlePLoS genetics2011

A large gene network in immature erythroid cells is controlled by the myeloid and B cell transcriptional regulator PU.1.

Sandeep N Wontakal, Xingyi Guo, Britta Will, Minyi Shi, Debasish Raha, Milind C Mahajan, Sherman Weissman, Michael Snyder, Ulrich Steidl, Deyou Zheng and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 51 citations in OpenAlex.

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  11. Runx1 promotes murine erythroid progenitor proliferation and inhibits differentiation by preventing Pu.1 downregulation.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

11 authors at 3 institutions in 1 country.

Sandeep N WontakalDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, United States of America.
Xingyi Guo
Britta Will
Minyi Shi
Debasish Raha
Milind C Mahajan
Sherman Weissman
Michael Snyder
Ulrich Steidl
Deyou Zheng
Arthur I Skoultchi
Albert Einstein College of Medicine · USYale University · USStanford University · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
PAX-6 AS A KEY REGULATOR OF LENS DEVELOPMENTR01EY012200 · NEI · YESHIVA UNIVERSITY · PI CVEKL, ALES · 2000 to 2025
$13.1M
Control of Erythroid Cell Division and DifferentiationR01HL078381 · NHLBI · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI SKOULTCHI, ARTHUR I · 2004 to 2008
$2.1M
Role of a Novel Homeobox Transcription Factor (HLX) in Acute Myeloid LeukemiaR01CA166429 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STEIDL, ULRICH · 2013 to 2017
$1.9M
Transcriptional regulation of leukemic stem cells in acute myeloid leukemiaR00CA131503 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI STEIDL, ULRICH · 2009 to 2011
$740k
NCI NIH HHS 2P30CA13330NCI NIH HHS HL078381/CA154239NCI NIH HHS P30 CA013330NCI NIH HHS R00 CA131503NCI NIH HHS R01 CA166429NEI NIH HHS EY012200NEI NIH HHS R01 EY012200NHLBI NIH HHS R01 HL078381NIGMS NIH HHS 5T32GM07288NIGMS NIH HHS T32 GM007288
6 · The paper itself

Abstract

PU.1 is a hematopoietic transcription factor that is required for the development of myeloid and B cells. PU.1 is also expressed in erythroid progenitors, where it blocks erythroid differentiation by binding to and inhibiting the main erythroid promoting factor, GATA-1. However, other mechanisms by which PU.1 affects the fate of erythroid progenitors have not been thoroughly explored. Here, we used ChIP-Seq analysis for PU.1 and gene expression profiling in erythroid cells to show that PU.1 regulates an extensive network of genes that constitute major pathways for controlling growth and survival of immature erythroid cells. By analyzing fetal liver erythroid progenitors from mice with low PU.1 expression, we also show that the earliest erythroid committed cells are dramatically reduced in vivo. Furthermore, we find that PU.1 also regulates many of the same genes and pathways in other blood cells, leading us to propose that PU.1 is a multifaceted factor with overlapping, as well as distinct, functions in several hematopoietic lineages.

Indexed as

Gene Regulatory NetworksTranscription, GeneticAnimalsCell DifferentiationCell LineCell LineageChromatin ImmunoprecipitationErythroid Precursor CellsMiceProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activators

Identifiers

PMID21695229
PMCPMC3111485
OpenAlexW1975400920

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.