ArticleJournal of molecular biology2007
Systematic RNAi studies on the role of Sp/KLF factors in globin gene expression and erythroid differentiation.
Article in Journal of molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- DNA G-quadruplex structures act as functional elements in α- and β-globin enhancers.Genome biology · 2025Article
- TF-Prioritizer: a Java pipeline to prioritize condition-specific transcription factors.GigaScience · 2022Article
- Erythroid lineage-specific lentiviral RNAi vectors suitable for molecular functional studies and therapeutic applications.Scientific reports · 2022Article
- Hemogen/BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis.Blood · 2022Article
- Integrative prediction of gene expression with chromatin accessibility and conformation data.Epigenetics & chromatin · 2020Article
- Nucleic Acid Therapy for β-Thalassemia.Biologics : targets & therapy · 2020Review
- MicroRNA‑9‑5p downregulates Klf4 and influences the progression of hepatocellular carcinoma via the AKT signaling pathway.International journal of molecular medicine · 2019Article
- Krüppel-like factor 8 induces epithelial-to-mesenchymal transition and promotes invasion of pancreatic cancer cells through transcriptional activation of four and a half LIM-only protein 2.Oncology letters · 2017Article
- Genome-scale high-resolution mapping of activating and repressive nucleotides in regulatory regions.Nature biotechnology · 2016Article
- MicroRNA Expression in β-Thalassemia and Sickle Cell Disease: A Role in The Induction of Fetal Hemoglobin.Cell journal · 2016Review
- Erythroid induction of K562 cells treated with mithramycin is associated with inhibition of raptor gene transcription and mammalian target of rapamycin complex 1 (mTORC1) functions.Pharmacological research · 2015Article
- A feedback loop consisting of microRNA 23a/27a and the β-like globin suppressors KLF3 and SP1 regulates globin gene expression.Molecular and cellular biology · 2013Article
- AAV6-mediated systemic shRNA delivery reverses disease in a mouse model of facioscapulohumeral muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- Inhibition of transcription factor specificity protein 1 alters the gene expression profile of keratinocytes leading to upregulation of kallikrein-related peptidases and thymic stromal lymphopoietin.The Journal of investigative dermatology · 2011Article
- Krüppel-like Factor 4 activates HBG gene expression in primary erythroid cells.British journal of haematology · 2011Article
- Regulation of the oncoprotein KLF8 by a switch between acetylation and sumoylation.American journal of translational research · 2011Article
- KLF8 recruits the p300 and PCAF co-activators to its amino terminal activation domain to activate transcription.Cell cycle (Georgetown, Tex.) · 2010Article
- A network of Krüppel-like Factors (Klfs). Klf8 is repressed by Klf3 and activated by Klf1 in vivo.The Journal of biological chemistry · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Sp/KLF family of factors regulates gene expression by binding to the CACCC/GC/GT boxes in the DNA through their highly conserved three zinc finger domains. To investigate the role of this family of factors in erythroid differentiation and globin gene expression, we first measured the expression levels of selected Sp/KLF factors in primary cells of fetal and adult stages of erythroid development. This quantitative analysis revealed that their expression levels vary significantly in cells of either stages of the erythroid development. Significant difference in their expression levels was observed between fetal and adult erythroid cells for some Sp/KLF factors. Functional studies using RNA interference revealed that the silencing of Sp1 and KLF8 resulted in elevated level of gamma globin expression in K562 cells. In addition, K562 cells become visibly red after Sp1 knockdown. Benzidine staining revealed significant hemoglobinization of these cells, indicating erythroid differentiation. Moreover, the expression of PU.1, ETS1 and Notch1 is significantly down-regulated in the cells that underwent erythroid differentiation following Sp1 knockdown. Overexpression of PU.1 or ETS1 efficiently blocked the erythroid differentiation caused by Sp1 knockdown in K562 cells. The expression of c-Kit, however, was significantly up-regulated. These data indicate that Sp1 may play an important role in erythroid differentiation.
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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.