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J. Cell Biol.,
Volume 141, Number 4, May 18, 1998 1041-1051
Institute for Molecular Pathology, A-1030 Vienna, Austria
The cytokine Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) regulates proliferation, differentiation, and apoptosis during myelopoiesis
and erythropoiesis. Structure-function relationships of
GM-CSF interactions with its receptor (GM-R), the
biochemistry of GM-R signal transduction, and GM-CSF action in vivo are relatively well understood. Much
less is known, however, about GM-R function in primary hematopoietic cells. In this paper we show that
expression of the human GM-R in a heterologous cell
system (primary avian erythroid and myeloid cells)
confirms respective results in murine or human cell
lines, but also provides new insights how the GM-R regulates progenitor proliferation and differentiation.
As expected, the hGM-CSF stimulated myeloid progenitor proliferation and differentiation and enhanced
erythroid progenitor proliferation during terminal differentiation. In the latter cells, however, the hGM-R
only partially substituted for the activities of the erythropoietin receptor (EpoR). It failed to replace the
EpoR in its cooperation with c-Kit to induce long-term
proliferation of erythroid progenitors. Furthermore,
the hGM-R 
chain specifically interfered with EpoR signaling, an activity neither seen for the 
c subunit of
the receptor complex alone, nor for the chain of the
closely related Interleukin-3 receptor. These results
point to a novel role of the GM-R chain in defining
cell type-specific functions of the GM-R.
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