|
|
 Previous Article | Table of Contents | Next Article 
Specific Signals Generated by the Cytoplasmic Domain of the Granulocyte
Colony-Stimulating Factor (G-CSF) Receptor Are Not Required for
G-CSF-Dependent Granulocytic Differentiation
Jason Jacob,
Jeffery S. Haug,
Sofia Raptis, and
Daniel C. Link
From the Division of Bone Marrow Transplantation and Stem Cell
Biology, Department of Medicine and Pathology, Washington University
Medical School, St Louis, MO.
Granulocyte colony-stimulating factor (G-CSF) is the principal
growth factor regulating the production of neutrophils, yet its role in
lineage commitment and terminal differentiation of hematopoietic
progenitor cells is controversial. In this study, we describe a system
to study the role of G-CSF receptor (G-CSFR) signals in granulocytic
differentiation using retroviral transduction of G-CSFR-deficient,
primary hematopoietic progenitor cells. We show that ectopic expression
of wild-type G-CSFR in hematopoietic progenitor cells supports
G-CSF-dependent differentiation of these cells into mature
granulocytes, macrophages, megakaryocytes, and erythroid cells.
Furthermore, we show that two mutant G-CSFR proteins, a truncation
mutant that deletes the carboxy-terminal 96 amino acids and a chimeric
receptor containing the extracellular and transmembrane domains of the
G-CSFR fused to the cytoplasmic domain of the erythropoietin receptor,
are able to support the production of morphologically mature,
chloroacetate esterase-positive, Gr-1/Mac-1-positive neutrophils in
response to G-CSF. These results demonstrate that ectopic expression of
the G-CSFR in hematopoietic progenitor cells allows for multilineage
differentiation and suggest that unique signals generated by the
cytoplasmic domain of the G-CSFR are not required for G-CSF-dependent
granulocytic differentiation.
Blood, Vol. 92 No. 2 (July 15), 1998:
pp. 353-361
© 1998 by the American Society of Hematology.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
C.-L. Hsu, K. Kikuchi, and M. Kondo
Activation of mitogen-activated protein kinase kinase (MEK)/extracellular signal regulated kinase (ERK) signaling pathway is involved in myeloid lineage commitment
Blood,
September 1, 2007;
110(5):
1420 - 1428.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
X. Lu, R. Levine, W. Tong, G. Wernig, Y. Pikman, S. Zarnegar, D. G. Gilliland, and H. Lodish
Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation
PNAS,
December 27, 2005;
102(52):
18962 - 18967.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. E. Lawlor, I. K. Campbell, D. Metcalf, K. O'Donnell, A. van Nieuwenhuijze, A. W. Roberts, and I. P. Wicks
Critical role for granulocyte colony-stimulating factor in inflammatory arthritis
PNAS,
August 3, 2004;
101(31):
11398 - 11403.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Shimizu, I. Kitabayashi, N. Kamada, T. Abe, N. Maseki, K. Suzukawa, and M. Ohki
AML1-MTG8 leukemic protein induces the expression of granulocyte colony-stimulating factor (G-CSF) receptor through the up-regulation of CCAAT/enhancer binding protein epsilon
Blood,
July 1, 2000;
96(1):
288 - 296.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. J. Szilvassy, T. E. Meyerrose, and B. Grimes
Effects of cell cycle activation on the short-term engraftment properties of ex vivo expanded murine hematopoietic cells
Blood,
May 1, 2000;
95(9):
2829 - 2837.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. G. Lutz, C. Moog-Lutz, E. Coumau-Gatbois, L. Kobari, Y. Di Gioia, and Y. E. Cayre
Myeloblastin is a granulocyte colony-stimulating factor-responsive gene conferring factor-independent growth to hematopoietic cells
PNAS,
February 15, 2000;
97(4):
1601 - 1606.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F.-C. Yang, K. Tsuji, A. Oda, Y. Ebihara, M.-j. Xu, A. Kaneko, S. Hanada, T. Mitsui, A. Kikuchi, A. Manabe, et al.
Differential Effects of Human Granulocyte Colony-Stimulating Factor (hG-CSF) and Thrombopoietin on Megakaryopoiesis and Platelet Function in hG-CSF Receptor-Transgenic Mice
Blood,
August 1, 1999;
94(3):
950 - 958.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
