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Article

CRISPR–Cas9-mediated gene editing of the BCL11A enhancer for pediatric β0/β0 transfusion-dependent β-thalassemia

1 Aug 2022

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Share to CRISPR and Genetic Engineering
Share to Hemoglobinopathies and Related Disorders
Share to Prenatal Screening and Diagnostics

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 35922667
DOI: 10.1038/s41591-022-01906-z

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CRISPR–Cas9-mediated gene editing of the BCL11A enhancer for pediatric β0/β0 transfusion-dependent β-thalassemiaPMID 35922667Read ↗

Targeted deletion of BCL11A gene by CRISPR-Cas9 system for fetal hemoglobin reactivation: A promising approach for gene therapy of beta thalassemia diseaseSemantic proximity Read ↗

CRISPR Gene Therapy: A Promising One-Time Therapeutic Approach for Transfusion-Dependent β-Thalassemia—CRISPR-Cas9 Gene Editing for β-ThalassemiaSemantic proximity Read ↗

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CRISPR-Cas9 Gene Editing for Sickle Cell Disease and β-ThalassemiaSemantic proximity Read ↗

Therapeutic gene editing strategies using CRISPR-Cas9 for the β-hemoglobinopathiesSemantic proximity Read ↗

Disruption of the BCL11A Erythroid Enhancer Reactivates Fetal Hemoglobin in Erythroid Cells of Patients with β-Thalassemia MajorSemantic proximity Read ↗

Advances in genome editing: the technology of choice for precise and efficient β-thalassemia treatmentSemantic proximity Read ↗

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