ArticleMolecular and cellular biology1995
The erythroid Krüppel-like factor transactivation domain is a critical component for cell-specific inducibility of a beta-globin promoter.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 122 citations in OpenAlex.
- Comprehensive regulation of γ-globin expression by epigenetic modifications and protein post-translational modifications.Clinical epigenetics · 2025Review
- Neomorphic effects of the neonatal anemia (Nan-Eklf) mutation contribute to deficits throughout development.Development (Cambridge, England) · 2017Article
- Therapeutic fetal-globin inducers reduce transcriptional repression in hemoglobinopathy erythroid progenitors through distinct mechanisms.Blood cells, molecules & diseases · 2016Article
- EKLF/KLF1, a tissue-restricted integrator of transcriptional control, chromatin remodeling, and lineage determination.Molecular and cellular biology · 2013Review
- ATP-dependent mitochondrial porphyrin importer ABCB6 protects against phenylhydrazine toxicity.The Journal of biological chemistry · 2012Article
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- Mammalian Krüppel-like factors in health and diseases.Physiological reviews · 2010Review
- Erythroid Kruppel-like factor (EKLF) is recruited to the gamma-globin gene promoter as a co-activator and is required for gamma-globin gene induction by short-chain fatty acid derivatives.European journal of haematology · 2009Article
- Failure of terminal erythroid differentiation in EKLF-deficient mice is associated with cell cycle perturbation and reduced expression of E2F2.Molecular and cellular biology · 2008Article
- Sumoylation of EKLF promotes transcriptional repression and is involved in inhibition of megakaryopoiesis.Molecular and cellular biology · 2007Article
- Altered regulation of beta-like globin genes by a redesigned erythroid transcription factor.Experimental hematology · 2007Article
- Alterations in expression and chromatin configuration of the alpha hemoglobin-stabilizing protein gene in erythroid Kruppel-like factor-deficient mice.Molecular and cellular biology · 2006Article
- The family feud: turning off Sp1 by Sp1-like KLF proteins.The Biochemical journal · 2005Review
- Stage-specific repression by the EKLF transcriptional activator.Molecular and cellular biology · 2004Article
- Identification of MoKA, a novel F-box protein that modulates Krüppel-like transcription factor 7 activity.Molecular and cellular biology · 2004Article
- Functional interplay between CBP and PCAF in acetylation and regulation of transcription factor KLF13 activity.Journal of molecular biology · 2003Article
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- Beta-globin locus control region HS2 and HS3 interact structurally and functionally.Nucleic acids research · 2003Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Erythroid Krüppel-like factor (EKLF) is an erythroid cell-specific DNA-binding protein that activates transcription from the beta-globin CACCC element, a functionally important and evolutionarily conserved component of globin as well as other erythroid cell-specific promoters and enhancers. We have attempted to elucidate the molecular role of EKLF in erythrocyte-specific transcriptional activation. First, in vivo and in vitro analyses have been used to demonstrate that the level of activation by EKLF is dependent on the orientation and number of CACCC elements, that EKLF contains separable activation and DNA-binding domains, and that the EKLF proline-rich region is a potent activator in CV-1 cells when fused to a nonrelated DNA-binding module. Second, we have established a transient assay in murine erythroleukemia cells in which reproducible levels of a reporter can be induced when linked to a locus control region enhancer-beta-globin promoter and in which induction is abolished when the promoter CAC site is mutated to a GAL site. Third, we demonstrate that the EKLF transactivation region, when fused to the GAL DNA-binding domain, can restore inducibility to this mutated construct and that this inducibility exhibits activator-, promoter-, and cell-type specificity. These results demonstrate that EKLF provides a crucial transactivation function for globin expression and further reinforce the idea that EKLF is an important regulator of CACCC element-directed transcription in erythroid cells.
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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.