Evidence map›Paper›PMID 28541545›Full record

ArticleNucleic acids research2017

Krüppel-like factors compete for promoters and enhancers to fine-tune transcription.

Melissa D Ilsley, Kevin R Gillinder, Graham W Magor, Stephen Huang, Timothy L Bailey, Merlin Crossley, Andrew C Perkins

Abstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
–field-weighted citation impact
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

46 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. KLF2 overrides the resident memory CD8 T cell differentiation program, in opposition to KLF3.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Genome-wide rules of transcription factor cooperativity revealed throughbioRxiv : the preprint server for biology · 2025
    Article
  12. CTCF regulates global chromatin accessibility and transcription during rod photoreceptor development.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Review
  14. KLF feedback loops in innate immunity.Frontiers in immunology · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. High-throughput screen identifies non inflammatory small molecule inducers of trained immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

7 authors.

Melissa D IlsleyMater Research Institute, Translational Research Institute, University of Queensland, Brisbane 4102, Australia.
Kevin R GillinderMater Research Institute, Translational Research Institute, University of Queensland, Brisbane 4102, Australia.
Graham W MagorMater Research Institute, Translational Research Institute, University of Queensland, Brisbane 4102, Australia.
Stephen HuangMater Research Institute, Translational Research Institute, University of Queensland, Brisbane 4102, Australia.
Timothy L BaileyCenter for Molecular Medicine, University of Nevada, Reno, NV, USA.
Merlin CrossleyUniversity of New South Wales, Sydney 1466, Australia.
Andrew C PerkinsMater Research Institute, Translational Research Institute, University of Queensland, Brisbane 4102, Australia.

Funding

The MEME Suite of motif-based sequence analysis toolsR01GM103544 · NIGMS · UNIVERSITY OF WASHINGTON · PI BAILEY, TIMOTHY L · 2012 to 2020
$2.4M
NIGMS NIH HHS R01 GM103544
6 · The paper itself

Abstract

Krüppel-like factors (KLFs) are a family of 17 transcription factors characterized by a conserved DNA-binding domain of three zinc fingers and a variable N-terminal domain responsible for recruiting cofactors. KLFs have diverse functions in stem cell biology, embryo patterning, and tissue homoeostasis. KLF1 and related family members function as transcriptional activators via recruitment of co-activators such as EP300, whereas KLF3 and related members act as transcriptional repressors via recruitment of C-terminal Binding Proteins. KLF1 directly activates the Klf3 gene via an erythroid-specific promoter. Herein, we show KLF1 and KLF3 bind common as well as unique sites within the erythroid cell genome by ChIP-seq. We show KLF3 can displace KLF1 from key erythroid gene promoters and enhancers in vivo. Using 4sU RNA labelling and RNA-seq, we show this competition results in reciprocal transcriptional outputs for >50 important genes. Furthermore, Klf3-/- mice displayed exaggerated recovery from anemic stress and persistent cell cycling consistent with a role for KLF3 in dampening KLF1-driven proliferation. We suggest this study provides a paradigm for how KLFs work in incoherent feed-forward loops or networks to fine-tune transcription and thereby control diverse biological processes such as cell proliferation.

Indexed as

Enhancer Elements, GeneticPromoter Regions, GeneticTranscriptional ActivationAnimalsCell LineCoculture TechniquesErythroid CellsErythropoiesisKruppel-Like Transcription FactorsMiceTranscription, Geneticerythroid Kruppel-like factorKlf3 protein, mouseKruppel-Like Transcription Factors

Identifiers

PMID28541545
PMCPMC5499887

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.