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March 22, 2026Open Access

Epigenomic Reactivation of Fetal Hemoglobin via BCL11A Enhancer Editing A Proposed Durable Strategy for Malaria Prevention

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Authors

DKdo gyeom Kim

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Overview

This proposal demonstrates a novel strategy to reactivate fetal hemoglobin for malaria prevention, suggesting an innovative approach to treatment.

Key Points

  • The research aims to develop a durable strategy for malaria prevention by reactivating fetal hemoglobin through epigenomic editing.
  • Utilized dCas9-DNMT3A-DNMT3L fusion protein for targeted editing.
  • Induced site-specific CpG methylation at the BCL11A enhancer.
  • Focused on hematopoietic stem cells (HSCs) for hemoglobin reactivation.
  • Successfully silenced the BCL11A repressor which impacts fetal hemoglobin levels.
  • Achieved effective methylation without traditional DNA breaks.
  • Demonstrated potential for long-lasting effects in malaria prevention.

Cite This Study

do gyeom Kim (2026) studied this question.

synapsesocial.com/papers/69bf898bf665edcd009e9457https://doi.org/10.5281/zenodo.19135549
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Silencing of BCL11A by disrupting enhancer-dependent epigenetic insulation2025 · 1 citations
  2. 2Targeted disruption of BCL11A ZnF4 enhances fetal hemoglobin in β-thalassemia and sickle cell disease: A druggable approach2025
  3. 3Recapitulating HPFH by CRISPR-Cas9 editing of γ-globin regulators to reactivate γ-globin expression2025
  4. 4Multiplex CRISPR/Cas9 genome editing in hematopoietic stem cells for fetal hemoglobin reinduction generates chromosomal translocations2021 · 51 citations
  5. 5CRISPR-directed epigenetic reprogramming of the FLT1 locus: a novel strategy for reversing fetal hemoglobin silencing in β-thalassemia minor2026