Cytokine-independent Jak3 Activation upon T Cell Receptor (TCR) Stimulation through Direct Association of Jak3 and the TCR Complex

Kazuhiro Tomita, Kaoru Saijo, Sho Yamasaki, Tomohiko Iida, Fubito Nakatsu, Hisashi Arase, Hiroshi Ohno, Takuji Shirasawa, Takayuki Kuriyama, John J. O'Shea, Takashi Saito

    研究成果: Contribution to journalArticle査読

    31 被引用数 (Scopus)

    抄録

    Jak3 is responsible for growth signals by various cytokines such as interleukin (IL)-2, IL-4, and IL-7 through association with the common γ chain (γc) 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/γc but is dependent on Lck and ZAP-70. Jak3 was found to be assembled with the TCR complex, particularly through direct association with CD3ζ via its JH4 region, which is a different region from that for γc 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.

    本文言語英語
    ページ(範囲)25378-25385
    ページ数8
    ジャーナルJournal of Biological Chemistry
    276
    27
    DOI
    出版ステータス出版済み - 7 6 2001

    All Science Journal Classification (ASJC) codes

    • 生化学
    • 分子生物学
    • 細胞生物学

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