PU.1 supports proliferation of immature erythroid progenitors

被引：22

作者：

Fisher, RC ^{[1
]}

Slayton, WB ^{[1
]}

Chien, C ^{[1
]}

Guthrie, SM ^{[1
]}

Bray, C ^{[1
]}

Scott, EW ^{[1
]}

机构：

[1] Univ Florida, Program Stem Cell Biol & Regenerat Med, Shands Canc Ctr, Dept Mol Genet & Microbiol, Gainesville, FL 32610 USA

来源：

LEUKEMIA RESEARCH | 2004年 / 28卷 / 01期

关键词：

PU; 1; transcription factor; erythropoiesis; synergy; erythropoietin; thrombopoietin; stem cell factor;

D O I：

10.1016/S0145-2126(03)00178-4

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Despite normal levels of erythropoiesis in PU.1(-/-) embryos, PU.1(-/-) fetal hematopoietic progenitors are unable to establish sustained erythropoiesis in the adult bone marrow. This study demonstrates that PU.1(-/-) fetal erythroid progenitors are synergistically expanded by TPO plus SCF, but not combinations of EPO plus SCF, IL-3 or GM-CSF The EPO defect is not corrected by a constitutively active variant of EPOR. Microarray analysis identified several candidate PU.1 target genes known to affect cytokine signaling and gene regulation in the erythroid lineage. These data suggest that PU.1 plays an important role in regulating the proliferation of immature erythroid progenitors. (C) 2003 Elsevier Ltd. All rights reserved.

引用

页码：83 / 89

页数：7

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