Home Abstract Introduction
Cross-linking Cell Lysis and DNA Fragmentation Chromatin immunoprecipitation and elution of DNA cross-link reversal and DNA Purification preparation of DNA for Sequencing Next Generation Sequencing process
KLF1 peaks Distance of promoter peaks Analysis of KLF1 binding to gene body of ZBTB7A

Website for translation of

Laura J. Norton, Alister P.W. Funnell (2017)
KLF1 directly activates expression of the novel fetal globin repressor ZBTB7A/LRF in erythroid cells
Blood Advances 1:685-692

(Translated by Wassal Alhammad)

Abstract

Sickle-cell anemia and β-thalassemia are widespread genetic diseases that are caused by the disruption of adult β-globin genes. As discovered from the Fetal Hemoglobin (HbF) analysis, reactivating this gene lead to significant amelioration of these diseases. It has been known that BCL11A represses the expression of fetal hemoglobin through direct activity of Kruppel-like transcription factor 1 (KLF1). A second layer of fetal hemoglobin repression is achieved by the activity of transcriptional factor repressor called ZBTB7A. Understanding the factors that regulate ZBTB7A expression has a direct impact on planning various therapeutic strategies to treat Sickle-cell anemia and β-thalassemia. In this website I intend to explain a major experiment that was conducted by Norton et.al to explore whether KLF1 regulates ZBTB7A by direct binding to its promoter.


Fig. 2: Consruction of How KLF1 and ZBTB7A work together: KLF1 increase ZBTB7A expression by binding to its gene promoter (top). ZBTB7A protein pinds to peta-globin promoter and prevent peta-globin gene from expression (bottom)