Abstract：
In their paper, using zebrafish models, Gioacchino et al. have demonstrated the GATA2 haploinsufficiency, the genetic hallmark of GATA2 deficiency syndrome, promotes erythroid and myeloid cytopenia, and have discovered a self-regulatory mechanism to compensate GATA2 levels and protein function. Commentary on: Gioacchino et al. GATA2 heterozygosity causes an epigenetic feedback mechanism resulting in myeloid and erythroid dysplasia. Br J Haematol 2024;205:580-593.
摘要：
在他们的论文中,使用斑马鱼模型，Gioacchinoetal.已经证明了GATA2单倍体不足，GATA2缺乏症的遗传标志，促进红细胞和骨髓细胞减少症，并发现了一种补偿GATA2水平和蛋白质功能的自我调节机制。评论：Gioacchino等人。GATA2杂合性导致表观遗传反馈机制，导致骨髓和红细胞发育异常。BrJHaematol2024（在线印刷）。doi:10.1111/bjh.19585。
