National Heart, Lung and Blood Institute/NIH, Sickle Cell Branch, Bethesda, USA.
National Heart, Lung and Blood Institute/NIH, Sickle Cell Branch, Bethesda, USA.
Gene. 2018 Jul 30;665:6-17. doi: 10.1016/j.gene.2018.04.065. Epub 2018 Apr 25.
MYB is a transcription factor which was identified in birds as a viral oncogene (v-MYB). Its cellular counterpart was subsequently isolated as c-MYB which has three functional domains - DNA binding domain, transactivation domain and negative regulatory domain. c-MYB is essential for survival, and deletion of both alleles of the gene results in embryonic death. It is highly expressed in hematopoietic cells, thymus and neural tissue, and required for T and B lymphocyte development and erythroid maturation. Additionally, aberrant MYB expression has been found in numerous solid cancer cells and human leukemia. Recent studies have also implicated c-MYB in the regulation of expression of fetal hemoglobin which is highly beneficial to the β-hemoglobinopathies (beta thalassemia and sickle cell disease). These findings suggest that MYB could be a potential therapeutic target in leukemia, and possibly also a target for therapeutic increase of fetal hemoglobin in the β-hemoglobinopathies.
MYB 是一种转录因子,最初在鸟类中被鉴定为病毒癌基因(v-MYB)。其细胞对应物随后被分离为 c-MYB,它具有三个功能域 - DNA 结合域、转录激活域和负调节域。c-MYB 对于生存是必需的,并且该基因的两个等位基因的缺失会导致胚胎死亡。它在造血细胞、胸腺和神经组织中高度表达,并且是 T 和 B 淋巴细胞发育和红细胞成熟所必需的。此外,异常的 MYB 表达已在许多实体癌细胞和人类白血病中发现。最近的研究还表明 c-MYB 参与调节胎儿血红蛋白的表达,这对β-血红蛋白病(β地中海贫血和镰状细胞病)非常有益。这些发现表明 MYB 可能是白血病的一个潜在治疗靶点,也可能是治疗β-血红蛋白病中胎儿血红蛋白增加的靶点。