Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion

Mohammad Ali Khosravi; Maryam Abbasalipour; Jean-Paul Concordet; Johannes Vom Berg; Sirous Zeinali; Arash Arashkia; Thorsten Buch; Morteza Karimipoor

doi:10.1016/j.dib.2019.104974

Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion

Data Brief. 2019 Dec 11:28:104974. doi: 10.1016/j.dib.2019.104974. eCollection 2020 Feb.

Authors

Mohammad Ali Khosravi^{1

2}, Maryam Abbasalipour¹, Jean-Paul Concordet³, Johannes Vom Berg², Sirous Zeinali¹, Arash Arashkia⁴, Thorsten Buch², Morteza Karimipoor¹

Affiliations

¹ Department of Molecular Medicine, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.
² Institute of Laboratory Animal Science, University of Zurich, Zurich, Switzerland.
³ Museum national d'Histoire naturelle, INSERM U1154, CNRS UMR 7196, Sorbonne Universites, 43 rue Cuvier, Paris, F-75231, France.
⁴ Department of Virology, Pasteur Institute of Iran, Tehran, Iran.

Abstract

The data presented in this article are related to the research article entitled as "Targeted deletion of the BCL11A gene by CRISPR-Cas9 system for fetal hemoglobin reactivation: A promising approach for gene therapy of beta-thalassemia disease " [1]. BCL11A is a master regulator of γ-globin gene silencing, and suppresses fetal hemoglobin expression by association with other γ-globin suppressors, and also interacts with human beta-globin locus control region as well as intergenic region between the Aγ and δ-globin genes to reconfigure beta-globin cluster. Thus, HbF reactivation has been proposed to be an approach for the treatment of β-thalassemia through knockout of BCL11A. Accordingly, an erythroid enhancer sequence was identified that, when inactivated, led to repression of BCL11A and induction of γ-globin in the erythroid lineage [2-7]. This article describes data that obtained from BCL11A gene enhancer modification in KU812 and KG-1 cell lines using the CRISPR-Cas9 genome editing system in order to reactivate γ-globin gene expression.

Keywords: BCL11A; CRISPR-Cas9 genome editing system; KG-1; KU812; γ-globin.