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Blood, Vol. 94 No. 1 (July 1), 1999:
pp. 74-86
Genetic Evidence for an Additional Factor Required for
Erythropoietin-Induced Signal Transduction
Sarah L. Gaffen,
Stephen Y. Lai,
Gregory D. Longmore,
Kathleen D. Liu, and
Mark A. Goldsmith
From the Gladstone Institute of Virology and Immunology, San
Francisco, CA; the Department of Medicine, School of Medicine,
University of California, San Francisco; and the Departments of
Medicine and Cell Biology, Washington University School of Medicine, St
Louis, MO.
Erythropoietin (EPO) and its receptor (EPOR) are required for the
development of mature erythrocytes. After binding of ligand, the EPOR
activates a variety of signaling pathways that ultimately control
cellular proliferation, survival, and specific gene expression. Although erythroid progenitors appear to be the principal
EPO-responsive cell type in vivo due to the restricted expression of
the EPOR, many growth factor-dependent cell lines expressing the EPOR
can respond to EPO by activating many or all of these pathways. In the
present study, we have identified a cellular context (the interleukin-2
[IL-2]-dependent HT-2 line) in which the EPO stimulation of the EPOR
fails to support cellular proliferation, STAT-5 induction, or MAPK
activation, despite efficient phosphorylation of the EPOR and JAK2 and
inhibition of apoptosis after withdrawal of IL-2. Interestingly, when
we fused HT-2 cells expressing the EPOR with Ba/F3 cells in a
complementation assay, the resulting hybridomas proliferated and
potently activated STAT-5 and MAPK in response to EPO. These data
indicate that an unidentified cellular factor is needed to mediate
signaling by the EPOR. Moreover, Ba/F3 cells apparently express this
factor(s) and somatic fusions can, therefore, confer EPO-responsiveness
to HT-2 cells that lack this factor.
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