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

来源：

LEUKEMIA | 2010年 / 24卷 / 07期

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

页码：1249 / 1257

页数：9

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