Evidence map›Paper›PMID 19704006›Full record

ArticleMolecular and cellular biology2009

Defective erythropoiesis in transgenic mice expressing dominant-negative upstream stimulatory factor.

Shermi Y Liang, Babak Moghimi, Valerie J Crusselle-Davis, I-Ju Lin, Michael H Rosenberg, Xingguo Li, John Strouboulis, Suming Huang, Jörg Bungert

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. DNA·RNA triple helix formation can function as aProceedings of the National Academy of Sciences of the United States of America · 2019
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  9. Neutralizing the function of a β-globin-associated cis-regulatory DNA element using an artificial zinc finger DNA-binding domain.Proceedings of the National Academy of Sciences of the United States of America · 2012
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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

9 authors at 3 institutions in 3 countries.

Shermi Y LiangDepartment of Biochemistry and Molecular Biology, College of Medicine, University of Florida, Gainesville, FL 32610, USA.
Babak Moghimi
Valerie J Crusselle-Davis
I-Ju Lin
Michael H Rosenberg
Xingguo Li
John Strouboulis
Suming Huang
Jörg Bungert
University of Florida · USInstitute of Genetics · HUAlexander Fleming Biomedical Sciences Research Center · GR

Funding

STRUCTURE/FUNCTION OF THE HUMAN B-GLOBIN LCRR01DK052356 · NIDDK · UNIVERSITY OF FLORIDA · PI BUNGERT, JORG · 1997 to 2017
$4.7M
Transcriptional regulation of TAL1/SCL in normal and malignant hematopoiesisR01HL090589 · NHLBI · UNIVERSITY OF FLORIDA · PI HUANG, SUMING · 2008 to 2012
$1.9M
NHLBI NIH HHS HL 090589NHLBI NIH HHS R01 HL090589NIDDK NIH HHS DK 52356NIDDK NIH HHS R01 DK052356
6 · The paper itself

Abstract

Transcription factor USF is a ubiquitously expressed member of the helix-loop-helix family of proteins. It binds with high affinity to E-box elements and, through interaction with coactivators, aids in the formation of transcription complexes. Previous work demonstrated that USF regulates genes during erythroid differentiation, including HoxB4 and beta-globin. Here, we show that the erythroid cell-specific expression of a dominant-negative mutant of USF, A-USF, in transgenic mice reduces the expression of all beta-type globin genes and leads to the diminished association of RNA polymerase II with locus control region element HS2 and with the beta-globin gene promoter. We further show that the expression of A-USF reduces the expression of several key erythroid cell-specific transcription factors, including EKLF and Tal-1. We provide evidence demonstrating that USF interacts with known regulatory DNA elements in the EKLF and Tal-1 gene loci in erythroid cells. Furthermore, A-USF-expressing transgenic mice exhibit a defect in the formation of CD71(+) progenitor and Ter-119(+) mature erythroid cells. In summary, the data demonstrate that USF regulates globin gene expression indirectly by enhancing the expression of erythroid transcription factors and directly by mediating the recruitment of transcription complexes to the globin gene locus.

Indexed as

Genes, DominantAnimalsAntigens, CDbeta-GlobinsChickensChromatin ImmunoprecipitationEmbryo, MammalianEmbryonic DevelopmentErythropoiesisGene Expression Regulation, DevelopmentalMiceMice, TransgenicModels, GeneticOrgan SpecificityPromoter Regions, GeneticProtein BindingAntigens, CDbeta-GlobinsCD71 antigenReceptors, TransferrinRNA Polymerase IITranscription FactorsUpstream Stimulatory Factors

Identifiers

PMID19704006
PMCPMC2772736
OpenAlexW2029119217

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.