|
|
 Previous Article | Table of Contents | Next Article 
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.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
C. Bose and K. B. Udupa
Erythropoietin enhancement of rat pancreatic tumor cell proliferation requires the activation of ERK and JNK signals
Am J Physiol Cell Physiol,
August 1, 2008;
295(2):
C394 - C405.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. J. Lindemann, Z. Hu, M. Benczik, K. D. Liu, and S. L. Gaffen
Differential Regulation of the IL-17 Receptor by {gamma}c Cytokines: INHIBITORY SIGNALING BY THE PHOSPHATIDYLINOSITOL 3-KINASE PATHWAY
J. Biol. Chem.,
May 16, 2008;
283(20):
14100 - 14108.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Ravid, I. Shams, N. Ben Califa, E. Nevo, A. Avivi, and D. Neumann
An extracellular region of the erythropoietin receptor of the subterranean blind mole rat Spalax enhances receptor maturation
PNAS,
September 4, 2007;
104(36):
14360 - 14365.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Um and H. F. Lodish
Antiapoptotic Effects of Erythropoietin in Differentiated Neuroblastoma SH-SY5Y Cells Require Activation of Both the STAT5 and AKT Signaling Pathways
J. Biol. Chem.,
March 3, 2006;
281(9):
5648 - 5656.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Lin, L. Brown, D. W. Hedley, D. L. Barber, and S. Benchimol
The death-promoting activity of p53 can be inhibited by distinct signaling pathways
Blood,
December 1, 2002;
100(12):
3990 - 4000.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Gala, A. Marreiros, G. J. Stewart, and P. Williamson
Overexpression of E2F-1 leads to cytokine-independent proliferation and survival in the hematopoietic cell line BaF-B03
Blood,
January 1, 2001;
97(1):
227 - 234.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. A. Ney and A. D. D'Andrea
Friend erythroleukemia revisited
Blood,
December 1, 2000;
96(12):
3675 - 3680.
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. B. Ehret, P. Reichenbach, U. Schindler, C. M. Horvath, S. Fritz, M. Nabholz, and P. Bucher
DNA Binding Specificity of Different STAT Proteins. COMPARISON OF IN VITRO SPECIFICITY WITH NATURAL TARGET SITES
J. Biol. Chem.,
February 23, 2001;
276(9):
6675 - 6688.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Sakamoto, T. Kitamura, and A. Yoshimura
Mitogen-activated Protein Kinase Plays an Essential Role in the Erythropoietin-dependent Proliferation of CTLL-2 Cells
J. Biol. Chem.,
November 10, 2000;
275(46):
35857 - 35862.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
