Evidence map›Paper›PMID 16705186›Full record

ArticleMolecular and cellular biology2006

Alterations in expression and chromatin configuration of the alpha hemoglobin-stabilizing protein gene in erythroid Kruppel-like factor-deficient mice.

Andre M Pilon, Douglas G Nilson, Dewang Zhou, Jose Sangerman, Tim M Townes, David M Bodine, Patrick G Gallagher

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

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  17. Severe anemia in the Nan mutant mouse caused by sequence-selective disruption of erythroid Kruppel-like factor.Proceedings of the National Academy of Sciences of the United States of America · 2010
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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

7 authors at 3 institutions in 1 country.

Andre M PilonHematopoiesis Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892-4442, USA.
Douglas G Nilson
Dewang Zhou
Jose Sangerman
Tim M Townes
David M Bodine
Patrick G Gallagher
National Institutes of Health · USUniversity of Alabama at Birmingham · USYale University · US

Funding

MOLECULAR BIOLOGY OF HUMAN ERYTHROCYTE ALPHA-SPECTRINR01HL065448 · NHLBI · YALE UNIVERSITY · PI GALLAGHER, PATRICK G · 2000 to 2013
$4.4M
Molecular Biology of Erythrocyte AnkyrinR01DK062039 · NIDDK · YALE UNIVERSITY · PI GALLAGHER, PATRICK G · 2002 to 2010
$3.3M
Genetic Modifers of Sickle Cell DiseaseR01HL068965 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI TOWNES, TIM M. · 2001 to 2005
$2.9M
Red Cell BiologyZ01HG200339 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BODINE, DAVID M. · 2007 to 2008
$2.3M
Gene Therapy for Hemoglobin DisordersZ01HG200340 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BODINE, DAVID M. · 2007 to 2008
$1.1M
Inproving gene transfer to provide intracellular immunizZ01HG000197 · NHGRI · HUMAN GENOME RESEARCH · PI BODINE, DAVID M. · 2001 to 2006
–
Intramural NIH HHSNHLBI NIH HHS HL65488NHLBI NIH HHS HL68965NHLBI NIH HHS R01 HL065448NHLBI NIH HHS R01 HL068965NIDDK NIH HHS DK/HL62039
6 · The paper itself

Abstract

Erythroid Krüppel-like factor (EKLF) is an erythroid zinc finger protein identified by its interaction with a CACCC sequence in the beta-globin promoter, where it establishes local chromatin structure permitting beta-globin gene transcription. We sought to identify other EKLF target genes and determine the chromatin status of these genes in the presence and absence of EKLF. We identified alpha hemoglobin-stabilizing protein (AHSP) by subtractive hybridization and demonstrated a 95 to 99.9% reduction in AHSP mRNA and the absence of AHSP in EKLF-deficient cells. Chromatin at the AHSP promoter from EKLF-deficient cells lacked a DNase I hypersensitive site and exhibited histone hypoacetylation across the locus compared to hyperacetylation of wild-type chromatin. Wild-type chromatin demonstrated a peak of EKLF binding over a promoter region CACCC box that differs from the EKLF consensus by a nucleotide. In mobility shift assays, the AHSP promoter CACCC site bound EKLF in a manner comparable to the beta-globin promoter CACCC site, indicating a broader recognition sequence for the EKLF consensus binding site. The AHSP promoter was transactivated by EKLF in K562 cells, which lack EKLF. These results support the hypothesis that EKLF acts as a transcription factor and a chromatin modulator for the AHSP and beta-globin genes and indicate that EKLF may play similar roles for other erythroid genes.

Indexed as

Gene Expression RegulationNucleic Acid ConformationAcetylationAnimalsBlood ProteinsChromatinHistonesHumansK562 CellsKruppel-Like Transcription FactorsMiceMolecular ChaperonesPromoter Regions, GeneticProtein BindingRegulatory Elements, TranscriptionalTranscriptional ActivationAhsp protein, mouseBlood ProteinsChromatinerythroid Kruppel-like factorHistonesKruppel-Like Transcription FactorsMolecular Chaperones

Identifiers

PMID16705186
PMCPMC1489081
OpenAlexW2110468079

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.