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Leuk Res. 2004 Jan;28(1):83-9.

PU.1 supports proliferation of immature erythroid progenitors.

Author information

1
Program in Stem Cell Biology and Regenerative Medicine, Shands Cancer Center, Department of Molecular Genetics and Microbiology, Box 100232, Room R4-293, University of Florida, Gainesville, FL 32610, USA. rbfisher@ufl.edu

Abstract

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.

PMID:
14630084
DOI:
10.1016/s0145-2126(03)00178-4
[Indexed for MEDLINE]

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