東京大学 · 医学
Mineo Kurokawa教授の研究室は、造血細胞の異常分化と白血病発症の分子機構に焦点を当てた研究を推進しています。特に、AML1/Evi-1やDNMT3A変異による腫瘍抑制経路の不活性化、TGF-βシグナルの抑制、ならびにエピジェネティクス的・シグナル伝達的制御の不全が白血球の異常増殖に与える影響を解明しています。細胞周期制御や幹細胞の自己複製能の異常に関連する分子機構の解明が、がん治療の新たな標的の発見に繋がると期待されています。
Figures are computed from collected data and may differ slightly.
The t(3;21)(q26;q22) chromosomal translocation associated with blastic crisis of chronic myelogenous leukemia results in the formation of the AML1/Evi-1 chimeric protein, which is thought to play a causative role in leukemic transformation of hematopoietic cells. Here we show that AML1/Evi-1 represses growth-inhibitory signaling by transforming growth factor-beta (TGF-beta) in 32Dcl3 myeloid cells. The activity of AML1/Evi-1 to repress TGF-beta signaling depends on the two separate regions of th
Despite the clinical impact of DNMT3A mutation on acute myeloid leukaemia, the molecular mechanisms regarding how this mutation causes leukaemogenesis in vivo are largely unknown. Here we show that, in murine transplantation experiments, recipients transplanted with DNMT3A mutant-transduced cells exhibit aberrant haematopoietic stem cell (HSC) accumulation. Differentiation-associated genes are downregulated without accompanying changes in methylation status of their promoter-associated CpG islan
The AML1 (RUNX1) gene, one of the most frequent targets of translocations associated with human leukemias, encodes a DNA-binding protein that plays pivotal roles in myeloid differentiation through transcriptional regulation of various genes. Previously, we reported that AML1 is phosphorylated on two serine residues with dependence on activation of extracellular signal-regulated kinase, which positively regulates the transcriptional activity of AML1. Here, we demonstrate that the interaction betw
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