Evidence map›Paper›PMID 19251649›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Distinct modes of gene regulation by a cell-specific transcriptional activator.

Tanushri Sengupta, Nathalie Cohet, François Morlé, James J Bieker

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-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

25 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. What do Transcription Factors Interact With?Journal of molecular biology · 2021
    Review
  5. Review
  6. Review
  7. AMolecular and cellular biology · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Transcription factor EKLF (KLF1) recruitment of the histone chaperone HIRA is essential for β-globin gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Structural and functional characterization of an atypical activation domain in erythroid Kruppel-like factor (EKLF).Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  19. Article
  20. Article
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

4 authors at 2 institutions in 2 countries.

Tanushri SenguptaDepartment of Developmental and Regenerative Biology, Mount Sinai School of Medicine, New York, NY 10029, USA.
Nathalie Cohet
François Morlé
James J Bieker
Centre National de la Recherche Scientifique · FRIcahn School of Medicine at Mount Sinai · US

Funding

Function of Putative Determinant in HematopoiesisR01DK046865 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI JAMES J BIEKER · 1993 to 2026
$11.2M
NIDDK NIH HHS R01 DK046865NIDDK NIH HHS R01 DK46865
6 · The paper itself

Abstract

The architectural layout of a eukaryotic RNA polymerase II core promoter plays a role in general transcriptional activation. However, its role in tissue-specific expression is not known. For example, differing modes of its recognition by general transcription machinery can provide an additional layer of control within which a single tissue-restricted transcription factor may operate. Erythroid Kruppel-like factor (EKLF) is a hematopoietic-specific transcription factor that is critical for the activation of subset of erythroid genes. We find that EKLF interacts with TATA binding protein-associated factor 9 (TAF9), which leads to important consequences for expression of adult beta-globin. First, TAF9 functionally supports EKLF activity by enhancing its ability to activate the beta-globin gene. Second, TAF9 interacts with a conserved beta-globin downstream promoter element, and ablation of this interaction by beta-thalassemia-causing mutations decreases its promoter activity and disables superactivation. Third, depletion of EKLF prevents recruitment of TAF9 to the beta-globin promoter, whereas depletion of TAF9 drastically impairs beta-promoter activity. However, a TAF9-independent mode of EKLF transcriptional activation is exhibited by the alpha-hemoglobin-stabilizing protein (AHSP) gene, which does not contain a discernable downstream promoter element. In this case, TAF9 does not enhance EKLF activity and depletion of TAF9 has no effect on AHSP promoter activation. These studies demonstrate that EKLF directs different modes of tissue-specific transcriptional activation depending on the architecture of its target core promoter.

Indexed as

Transcriptional Activationbeta-Globinsbeta-ThalassemiaBlood ProteinsGene Expression RegulationHumansKruppel-Like Transcription FactorsMolecular ChaperonesMutationPromoter Regions, GeneticTATA-Binding Protein Associated FactorsTissue DistributionTranscription FactorsTranscription Factor TFIIDAHSP protein, humanbeta-GlobinsBlood Proteinserythroid Kruppel-like factorKruppel-Like Transcription FactorsMolecular ChaperonesTAF9 protein, humanTATA-Binding Protein Associated FactorsTranscription FactorsTranscription Factor TFIID

Identifiers

PMID19251649
PMCPMC2657397
OpenAlexW2020204285

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.