ArticleMolecular and cellular biology2012
The CACCC-binding protein KLF3/BKLF represses a subset of KLF1/EKLF target genes and is required for proper erythroid maturation in vivo.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
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- Maternal diet alters long-term innate immune cell memory in fetal and juvenile hematopoietic stem and progenitor cells in nonhuman primate offspring.Cell reports · 2023Article
- Pan-cancer analysis of Krüppel-like factor 3 and its carcinogenesis in pancreatic cancer.Frontiers in immunology · 2023Article
- Tissue-Specific Variations in Transcription Factors Elucidate Complex Immune System Regulation.Genes · 2022Article
- PRKCE non-coding variants influence on transcription as well as translation of its gene.RNA biology · 2022Article
- Article
- Eosinophil function in adipose tissue is regulated by Krüppel-like factor 3 (KLF3).Nature communications · 2020Article
- Krüppel-like factor 3 (KLF3) suppresses NF-κB-driven inflammation in mice.The Journal of biological chemistry · 2020Article
- Expression of human Krüppel-like factor 3 in peripheral blood as a promising biomarker for acute leukemia.Cancer medicine · 2020Article
- MiR-326/Sp1/KLF3: A novel regulatory axis in lung cancer progression.Cell proliferation · 2019Article
- Krüppel-like factors: Crippling and un-crippling metabolic pathways.JACC. Basic to translational science · 2018Article
- Krüppel-like factors compete for promoters and enhancers to fine-tune transcription.Nucleic acids research · 2017Article
- Direct competition between DNA binding factors highlights the role of Krüppel-like Factor 1 in the erythroid/megakaryocyte switch.Scientific reports · 2017Article
- KLF1 directly activates expression of the novel fetal globin repressorBlood advances · 2017Article
- Krüppel-like Factor 3 (KLF3/BKLF) Is Required for Widespread Repression of the Inflammatory Modulator Galectin-3 (Lgals3).The Journal of biological chemistry · 2016Article
- Phosphorylation of Krüppel-like factor 3 (KLF3/BKLF) and C-terminal binding protein 2 (CtBP2) by homeodomain-interacting protein kinase 2 (HIPK2) modulates KLF3 DNA binding and activity.The Journal of biological chemistry · 2015Article
- Krüppel-like transcription factors KLF1 and KLF2 have unique and coordinate roles in regulating embryonic erythroid precursor maturation.Haematologica · 2014Article
- Differential regulation of the α-globin locus by Krüppel-like Factor 3 in erythroid and non-erythroid cells.BMC molecular biology · 2014Article
- Repression of chimeric transcripts emanating from endogenous retrotransposons by a sequence-specific transcription factor.Genome biology · 2014Article
- Regions outside the DNA-binding domain are critical for proper in vivo specificity of an archetypal zinc finger transcription factor.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CACCC-box binding protein erythroid Krüppel-like factor (EKLF/KLF1) is a master regulator that directs the expression of many important erythroid genes. We have previously shown that EKLF drives transcription of the gene for a second KLF, basic Krüppel-like factor, or KLF3. We have now tested the in vivo role of KLF3 in erythroid cells by examining Klf3 knockout mice. KLF3-deficient adults exhibit a mild compensated anemia, including enlarged spleens, increased red pulp, and a higher percentage of erythroid progenitors, together with elevated reticulocytes and abnormal erythrocytes in the peripheral blood. Impaired erythroid maturation is also observed in the fetal liver. We have found that KLF3 levels rise as erythroid cells mature to become TER119(+). Consistent with this, microarray analysis of both TER119(-) and TER119(+) erythroid populations revealed that KLF3 is most critical at the later stages of erythroid maturation and is indeed primarily a transcriptional repressor. Notably, many of the genes repressed by KLF3 are also known to be activated by EKLF. However, the majority of these are not currently recognized as erythroid-cell-specific genes. These results reveal the molecular and physiological function of KLF3, defining it as a feedback repressor that counters the activity of EKLF at selected target genes to achieve normal erythropoiesis.
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