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J. Biol. Chem., Vol. 276, Issue 27, 25378-25385, July 6, 2001
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From the Jak3 is responsible for growth signals by various
cytokines such as interleukin (IL)-2, IL-4, and IL-7 through
association with the common
Cytokine-independent Jak3 Activation upon T Cell
Receptor (TCR) Stimulation through Direct Association of Jak3 and
the TCR Complex*
§,¶,,§,,
,**,,¶¶
Department of Molecular Genetics, Chiba
University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba
260-8790, the Department of
Neurophysiology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo 173-0015, the § Department of
Internal Medicine, Institute of Pulmonary Cancer Research, School of
Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8790, Japan, the §§ Lymphocyte Cell Biology Section,
NIAMS, National Institutes of Health,
Bethesda, Maryland 20892-1820
chain (c) in lymphocytes. We found
that T cells from Jak3-deficient mice exhibit impairment of not only
cytokine signaling but also early activation signals and that Jak3 is
phosphorylated upon T cell receptor (TCR) stimulation. TCR-mediated
phosphorylation of Jak3 is independent of IL-2 receptor/c but is
dependent on Lck and ZAP-70. Jak3 was found to be assembled with the
TCR complex, particularly through direct association with CD3
via
its JH4 region, which is a different region from that for c
association. These results suggest that Jak3 plays a role not only in
cell growth but also in T cell activation and represents cross-talk of
a signaling molecule between TCR and growth signals.
*
This work was supported by a grant-in-aid for scientific
research from the Ministry of Education of Japan and a grant from the
Human Frontier Scientific Program.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.
Present address: Dept. of Microbiology and Immunology,
Univ. of California, San Francisco, 152 Parnassus Ave., San
Francisco, CA 94143.
**
Present address: Div. of Molecular Membrane Biology, Cancer
Research Institute, Kanazawa University, 13-1 Takaramachi,
Kanazawa 920-0934, Japan.
¶¶
To whom correspondence should be addressed. Tel.:
81-43-226-2198; Fax: 81-43-222-1791; E-mail:
saito@med.m.chiba-u.ac.jp.
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