Ryo Kurita

This study identifies the transcriptional regulatory mechanisms governing ERFE expression in human erythroblasts using genomic approaches.

This study demonstrates the use of base editors to precisely correct various β-thalassemic mutations in human erythroid cells, showing efficient and scarless mutation correction with normal hemoglobin variants.

This study uses CRISPR base editing to identify novel mutations in the HBG promoter that increase fetal hemoglobin expression without harmful effects.

The paper shows that deleting the 3HS1 CTCF binding site increases fetal hemoglobin expression in hematopoietic stem cells and erythroid progenitor cells, suggesting therapeutic potential for hemoglobinopathies.

The paper develops a platform combining ATAC-seq, DNaseI footprints, NG Capture-C, and machine learning to identify causal variants and genes for polygenic human traits.

This study uses CRISPR-Cas9 to test a putative fetal globin repressor region, finding it does not autonomously silence gamma-globin, suggesting it is not a therapeutic target for beta-hemoglobinopathies.

The paper identifies BAP1 as a key repressor of fetal hemoglobin biosynthesis by maintaining NCoR1 at the β-globin locus and shows its inhibition increases γ-globin synthesis.