The 75-kD HS1 protein is highly tyrosine-phosphorylated during B cell antigen receptor (BCR)-mediated signaling. Owing to low expression of HS1, WEHI-231-derived M1 cells, unlike the parental cells, are insensitive to BCR-mediated apoptosis. Here, we show that BCR-associated tyrosine kinases Lyn and Syk synergistically phosphorylate HS1, and that Tyr378 and Tyr-397 of HS1 are the critical residues for its BCR-induced phosphorylation. In addition, unlike wild-type HS1, a mutant HS1 carrying the mutations Phe-378 and Phe-397 was unable to render M1 cells sensitive to apoptosis. Wild-type HS1, but not the mutant, localized to the nucleus under the synergy of Lyn and Syk. Thus, tyrosine phosphorylation of HS1 is required for BCR-induced apoptosis and nuclear translocation of HS1 may be a prerequisite for B cell apoptosis.
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7 April 1997
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April 07 1997
Role of Tyrosine Phosphorylation of HS1 in B Cell Antigen Receptor-mediated Apoptosis
Yuji Yamanashi,
Yuji Yamanashi
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Takahiro Fukuda,
Takahiro Fukuda
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Hirofumi Nishizumi,
Hirofumi Nishizumi
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Tetsuya Inazu,
Tetsuya Inazu
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Ken-ichi Higashi,
Ken-ichi Higashi
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Daisuke Kitamura,
Daisuke Kitamura
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Takaomi Ishida,
Takaomi Ishida
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Hirohei Yamamura,
Hirohei Yamamura
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Takeshi Watanabe,
Takeshi Watanabe
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Tadashi Yamamoto
Tadashi Yamamoto
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
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Yuji Yamanashi
,
Takahiro Fukuda
,
Hirofumi Nishizumi
,
Tetsuya Inazu
,
Ken-ichi Higashi
,
Daisuke Kitamura
,
Takaomi Ishida
,
Hirohei Yamamura
,
Takeshi Watanabe
,
Tadashi Yamamoto
From the *Department of Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan; ‡Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-62, Japan; §Department of Biochemistry, Fukui Medical School, Fukui 910-11, Japan; ‖Research Institute for Bioscience, Science University of Tokyo, Noda 278, Japan; and the ¶Department of Biochemistry, Kobe University, School of Medicine, Kobe 650, Japan
Address correspondence to Tadashi Yamamoto, Department of Oncology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108, Japan. The current address for Y. Yamanashi is the Department of Biology, MIT, 77 Massachusetts Ave., Cambridge, MA 02139.
Received:
August 05 1996
Revision Received:
January 29 1997
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1997
J Exp Med (1997) 185 (7): 1387–1392.
Article history
Received:
August 05 1996
Revision Received:
January 29 1997
Citation
Yuji Yamanashi, Takahiro Fukuda, Hirofumi Nishizumi, Tetsuya Inazu, Ken-ichi Higashi, Daisuke Kitamura, Takaomi Ishida, Hirohei Yamamura, Takeshi Watanabe, Tadashi Yamamoto; Role of Tyrosine Phosphorylation of HS1 in B Cell Antigen Receptor-mediated Apoptosis. J Exp Med 7 April 1997; 185 (7): 1387–1392. doi: https://doi.org/10.1084/jem.185.7.1387
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