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J Biol Chem, Vol. 273, Issue 28, 17742-17748, July 10, 1998
From the Departments of Exposure of B-lineage lymphoid cells to ionizing
radiation induces an elevation of c-jun proto-oncogene
mRNA levels. This signal is abrogated by protein-tyrosine kinase
(PTK) inhibitors, indicating that activation of an as yet unidentified
PTK is mandatory for radiation-induced c-jun expression.
Here, we provide experimental evidence that the cytoplasmic tyrosine
kinases BTK, SYK, and LYN are not required for this signal. Lymphoma
B-cells rendered deficient for LYN, SYK, or both by targeted gene
disruption showed increased c-jun expression levels after
radiation exposure, but the magnitude of the stimulation was lower than
in wild-type cells. Thus, these PTKs may participate in the generation
of an optimal signal. Notably, an inhibitor of JAK-3 (Janus
family kinase-3) abrogated radiation-induced c-jun activation, prompting the hypothesis that a chicken
homologue of JAK-3 may play a key role in initiation of the
radiation-induced c-jun signal in B-lineage lymphoid
cells.
Role of Tyrosine Kinases in Induction of the c-jun
Proto-oncogene in Irradiated B-lineage Lymphoid Cells
,, and Molecular Genetics and
§ Molecular Oncology, Wayne Hughes Institute,
St. Paul, Minnesota 55113
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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