ArticleMolecular and cellular biology2001
Unanticipated repression function linked to erythroid Krüppel-like factor.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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.
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.
Who cites it
36 citing papers in PubMed, 76 citations in OpenAlex.
- Erythroid Krüppel-Like Factor (KLF1): A Surprisingly Versatile Regulator of Erythroid Differentiation.Advances in experimental medicine and biology · 2024Review
- Predicting 3D Structure, Cross Talks, and Prognostic Significance ofFrontiers in oncology · 2021Article
- Lysine Acetylation Goes Global: From Epigenetics to Metabolism and Therapeutics.Chemical reviews · 2018Review
- New PAH gene promoter KLF1 and 3'-region C/EBPalpha motifs influence transcription in vitro.Journal of applied genetics · 2017Article
- Review
- The DEK Oncoprotein Is a Critical Component of the EKLF/KLF1 Enhancer in Erythroid Cells.Molecular and cellular biology · 2015Article
- SOX9 inhibits β-TrCP-mediated protein degradation to promote nuclear GLI1 expression and cancer stem cell properties.Journal of cell science · 2015Article
- Generation of mice deficient in both KLF3/BKLF and KLF8 reveals a genetic interaction and a role for these factors in embryonic globin gene silencing.Molecular and cellular biology · 2013Article
- Klf10 inhibits IL-12p40 production in macrophage colony-stimulating factor-induced mouse bone marrow-derived macrophages.European journal of immunology · 2013Article
- EKLF/KLF1, a tissue-restricted integrator of transcriptional control, chromatin remodeling, and lineage determination.Molecular and cellular biology · 2013Review
- Novel roles for KLF1 in erythropoiesis revealed by mRNA-seq.Genome research · 2012Article
- Review
- Review
- Krüppel-like Factor 4 activates HBG gene expression in primary erythroid cells.British journal of haematology · 2011Article
- Dose-dependent regulation of primitive erythroid maturation and identity by the transcription factor Eklf.Blood · 2010Article
- Mammalian Krüppel-like factors in health and diseases.Physiological reviews · 2010Review
- EKLF directly activates the p21WAF1/CIP1 gene by proximal promoter and novel intronic regulatory regions during erythroid differentiation.Molecular and cellular biology · 2010Article
- Nonhistone protein acetylation as cancer therapy targets.Expert review of anticancer therapy · 2010Review
- Advances in the understanding of haemoglobin switching.British journal of haematology · 2010Review
- Differential requirement of a distal regulatory region for pre-initiation complex formation at globin gene promoters.Nucleic acids research · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The erythroid cell-specific transcription factor erythroid Krüppel-like factor (EKLF) is an important activator of beta-globin gene expression. It achieves this by binding to the CACCC element at the beta-globin promoter via its zinc finger domain. The coactivators CBP and P300 interact with, acetylate, and enhance its activity, helping to explain its role as a transcription activator. Here we show that EKLF can also interact with the corepressors mSin3A and HDAC1 (histone deacetylase 1) through its zinc finger domain. When linked to a GAL4 DNA binding domain, full-length EKLF or its zinc finger domain alone can repress transcription in vivo. This repressive activity can be relieved by the HDAC inhibitor trichostatin A. Although recruitment of EKLF to a promoter is required to show repression, its zinc finger domain cannot bind directly to DNA and repress transcription simultaneously. In addition, the target promoter configuration is important for enabling EKLF to exhibit any repressive activity. These results suggest that EKLF may function in vivo as a transcription repressor and play a previously unsuspected additional role in regulating erythroid gene expression and differentiation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.