GATA2 deficiency syndrome: A compensatory mechanism gone awry?

被引:0
|
作者
Rio-Machin, Ana [1 ,2 ]
机构
[1] IIS Fdn Jimenez Diaz, UAM, Expt Hematol Lab, Madrid, Spain
[2] Queen Mary Univ London, Barts Canc Inst, Ctr Haemato Oncol, London, England
关键词
acute leukaemia; gene expression; genetic disorders; immunodeficiency; MDS; EXPRESSION;
D O I
10.1111/bjh.19638
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 (Online ahead of print). doi: 10.1111/bjh.19585.
引用
收藏
页码:411 / 413
页数:3
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