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


Khosravi, Mohammad Ali; Abbasalipour, Maryam; Concordet, Jean-Paul; Berg, Johannes vom; Zeinali, Sirous; Arashkia, Arash; Buch, Thorsten; Karimipoor, Morteza (2019). Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion. Data in Brief, 28:104974.

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.

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.

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Additional indexing

Contributors:Stanislav Pantelyushin for his support in the lab of Prof. Buch
Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Laboratory Animal Science
05 Vetsuisse Faculty > Institute of Laboratory Animal Science
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Uncontrolled Keywords:Multidisciplinary, BCL11A; CRISPR-Cas9 genome editing system; KG-1; KU812; γ-globin
Language:English
Date:1 December 2019
Deposited On:06 Jan 2020 16:59
Last Modified:07 Jan 2020 08:36
Publisher:Elsevier
ISSN:2352-3409
OA Status:Gold
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.dib.2019.104974
PubMed ID:31890812
Project Information:
  • : FunderPasteur Institute of Iran
  • : Grant IDgrant number: BP-9035
  • : Project Title

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