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Tec and Jak2 Kinases Cooperate to Mediate Cytokine-Driven
Activation of c-fos Transcription
Yoshihiro Yamashita,
Sumiko Watanabe,
Akira Miyazato,
Ken-ichi Ohya,
Uichi Ikeda,
Kazuyuki Shimada,
Norio Komatsu,
Kiyohiko Hatake,
Yasusada Miura,
Keiya Ozawa, and
Hiroyuki Mano
From the Department of Molecular Biology, the Divisions of Hematology
and Cardiology, Jichi Medical School, Tochigi; and the Department of
Molecular and Developmental Biology, Institute of Medical Science,
University of Tokyo, Tokyo, Japan.
Although transcriptional activation of the c-fos
proto-oncogene plays an intrinsic role in the mechanism of blood cell
growth, it is still obscure how protein-tyrosine kinases (PTKs)
regulate the cytokine-driven c-fos activation
pathway. We present here that Tec PTK is
tyrosine-phosphorylated and activated by granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation in a human
GM-CSF-dependent cell line. Moreover, we could show that introduction
of Tec into mouse BA/F3-hGMR  cells can profoundly activate the
c-fos promoter in response to GM-CSF or to interleukin-3
(IL-3). In contrast, introduction of a kinase-deleted Tec could
suppress cytokine-driven c-fos activation, indicating that Tec
is directly involved in the regulation of c-fos transcription.
Interestingly, strong activation by Tec of the c-fos promoter
was blocked by the co-expression of dominant negative Jak2. The
molecular interaction between Tec and Jak2 was then investigated both
in mammalian and insect cell systems, revealing that they can not only
bind to each other, but either of the two can phosphorylate the other.
Thus, Tec and Jak2 can "cross-talk" in a complexed way to mediate
cytokine-driven c-fos activation.
Blood, Vol. 91 No. 5 (March 1), 1998:
pp. 1496-1507
© 1998 by The American Society of Hematology.
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