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J. Biol. Chem., Vol. 275, Issue 38, 29275-29282, September 22, 2000
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From the The SH2-containing inositol 5'-phosphatase (SHIP)
is tyrosine-phosphorylated in response to cytokines such as interleukin (IL)-3, granulocyte-macrophage colony-stimulating factor, and macrophage colony-stimulating factor. SHIP has been shown to modulate negatively these cytokine signalings; however, a potential role in IL-4
signaling remains uncharacterized. It has been recently shown that IL-4
induces tyrosine phosphorylation of SHIP, implicating the phosphatase
in IL-4 processes. Tyrosine kinases, Jak1 and Jak3, involved in
IL-4 signaling can associate with SHIP, yet only Jak1 can
tyrosine-phosphorylate SHIP when co-expressed. In functional studies,
cells overexpressing wild type SHIP are found to be hyperproliferative
in response to IL-4 in comparison to parental cells. In contrast, cells
expressing catalytically inactive form, SHIP(D672A), show reduced
proliferation in response to IL-4. These changes in IL-4-induced
proliferation correlate with alterations in phosphatidylinositol
3,4,5-triphosphate levels. However, no differential activation of
STAT6, Akt, IRS-2, or p70S6k, in response to IL-4,
was observed in these cells. These data suggest that the catalytic
activity of SHIP acts in a novel manner to influence IL-4 signaling. In
addition, these data support recent findings that suggest there are
uncharacterized signaling pathways downstream of phosphatidylinositol
3,4,5-triphosphate.
Positive Regulation of Interleukin-4-mediated Proliferation by
the SH2-containing Inositol-5'-phosphatase*
§¶,§,,,
,§§, and§§¶¶
Departments of Medicine and Microbiology,
Columbia University, College of Physicians and Surgeons,
New York, New York 10032, the ** Department of Immunology, National
Jewish Medical and Research Center, Denver, Colorado 80206, and the
Department of Microbiology, Ohio State
University, Columbus, Ohio 43210
*
This work was supported in part by National Institutes of
Health Grants AI33450, CA64628, AI41447, and 2T32DK07328 and a grant from the Asthma and Allergy Foundation of America.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by a Cancer Research Institute fellowship.
§§
Scholars of the Leukemia Society of America.
¶¶
To whom correspondence should be addressed: Columbia
University, 630 W. 168th St., P&S 8-425, New York, NY 10032. Tel.:
212-305-1984; Fax: 212-305-1870; E-mail: pbr3@columbia.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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