Ryo Kurita

Regulation of Human Erythroferrone Expression

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

Precise modelling and correction of a spectrum of β-thalassemic mutations in human erythroid cells by base editors

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.

Identification of novel HPFH-like mutations by CRISPR base editing that elevates the expression of fetal hemoglobin

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

3'HS1 CTCF binding site in human β-globin locus regulates fetal hemoglobin expression

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.

An integrated platform to systematically identify causal variants and genes for polygenic human traits.

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.

CRISPR-Cas9 interrogation of a putative fetal globin repressor in human erythroid cells.

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.

BAP1 deubiquitinase is a potent repressor of fetal hemoglobin biosynthesis

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.