Evidence map›Paper›PMID 14559995›Full record

ArticleMolecular and cellular biology2003

PU.1 and pRB interact and cooperate to repress GATA-1 and block erythroid differentiation.

Natasha Rekhtman, Kevin S Choe, Igor Matushansky, Stuart Murray, Tomas Stopka, Arthur I Skoultchi

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

53 citing papers in PubMed, 100 citations in OpenAlex.

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  15. Molecular ties between the cell cycle and differentiation in embryonic stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2014
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  18. H1 linker histone promotes epigenetic silencing by regulating both DNA methylation and histone H3 methylation.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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

6 authors at 1 institution in 1 country.

Natasha RekhtmanDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Kevin S Choe
Igor Matushansky
Stuart Murray
Tomas Stopka
Arthur I Skoultchi
Albert Einstein College of Medicine · 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
CONTROL OF DIFFERENTIATION OF ERYTHROLEUKEMIC CELLSR37CA016368 · NCI · YESHIVA UNIVERSITY · PI SKOULTCHI, ARTHUR I · 1990 to 1997
–
NCI NIH HHS 2P30CA13330NCI NIH HHS 5R37CA16368NCI NIH HHS P30 CA013330NIGMS NIH HHS 5T32GM07288-25NIGMS NIH HHS T32 GM007288
6 · The paper itself

Abstract

PU.1 and GATA-1 are two hematopoietic specific transcription factors that play key roles in development of the myeloid and erythroid lineages, respectively. The two proteins bind to one another and inhibit each other's function in transcriptional activation and promotion of their respective differentiation programs. This mutual antagonism may be an important aspect of lineage commitment decisions. PU.1 can also act as an oncoprotein since deregulated expression of PU.1 in erythroid precursors causes erythroleukemias in mice. Studies of cultured mouse erythroleukemia cell lines indicate that one aspect of PU.1 function in erythroleukemogenesis is its ability to block erythroid differentiation by repressing GATA-1 (N. Rekhtman, F. Radparvar, T. Evans, and A. I. Skoultchi, Genes Dev. 13:1398-1411, 1999). We have investigated the mechanism of PU.1-mediated repression of GATA-1. We report here that PU.1 binds to GATA-1 on DNA. We localized the repression activity of PU.1 to a small acidic N-terminal domain that interacts with the C pocket of pRB, a well-known transcriptional corepressor. Repression of GATA-1 by PU.1 requires pRB, and pRB colocalizes with PU.1 and GATA-1 at repressed GATA-1 target genes. PU.1 and pRB also cooperate to block erythroid differentiation. Our results suggest that one of the mechanisms by which PU.1 antagonizes GATA-1 is by binding to it at GATA-1 target genes and tethering to these sites a corepressor that blocks transcriptional activity and thereby erythroid differentiation.

Indexed as

AnimalsBinding SitesCell DifferentiationCell LineCell LineageDNA-Binding ProteinsErythroid Precursor CellsErythroid-Specific DNA-Binding FactorsGATA1 Transcription FactorGene Expression RegulationGenes, ReporterHumansMiceProtein BindingProtein Structure, TertiaryProto-Oncogene ProteinsDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsGATA1 protein, humanGata1 protein, mouseGATA1 Transcription FactorProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Recombinant Fusion ProteinsRetinoblastoma ProteinTrans-ActivatorsTranscription Factors

Identifiers

PMID14559995
PMCPMC207581
OpenAlexW2159680972

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.