The role of PU.1 and GATA-1 transcription factors during normal and leukemogenic hematopoiesis

被引:126
作者
Burda, P. [1 ,2 ]
Laslo, P. [3 ]
Stopka, T. [1 ,2 ,4 ]
机构
[1] Charles Univ Prague, Dept Pathophysiol, Fac Med 1, Prague 12853 2, Czech Republic
[2] Charles Univ Prague, Ctr Expt Hematol, Fac Med 1, Prague 12853 2, Czech Republic
[3] Univ Leads, Sect Expt Haematol, Leeds Inst Mol Med, St Jamess Univ Hosp, Leeds, W Yorkshire, England
[4] Gen Univ Hosp, Dept Med Hematol 1, Prague, Czech Republic
基金
英国惠康基金;
关键词
PU.1; leukemia differentiation; GATA-1; chromatin; differentiation therapy; ACUTE MYELOID-LEUKEMIA; LINEAGE COMMITMENT; RETINOIC ACID; C/EBP-ALPHA; HISTONE DEACETYLASE; GENE-EXPRESSION; STEM-CELLS; TERMINAL DIFFERENTIATION; ERYTHROLEUKEMIA-CELLS; REGULATORY NETWORK;
D O I
10.1038/leu.2010.104
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Hematopoiesis is coordinated by a complex regulatory network of transcription factors and among them PU.1 (Spi1, Sfpi1) represents a key molecule. This review summarizes the indispensable requirement of PU.1 during hematopoietic cell fate decisions and how the function of PU.1 can be modulated by protein-protein interactions with additional factors. The mutual negative regulation between PU.1 and GATA-1 is detailed within the context of normal and leukemogenic hematopoiesis and the concept of 'differentiation therapy' to restore normal cellular differentiation of leukemic cells is discussed. Leukemia (2010) 24, 1249-1257; doi:10.1038/leu.2010.104; published online 3 June 2010
引用
收藏
页码:1249 / 1257
页数:9
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