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(Received for publication, October 10, 1995)
The c-Jun N-terminal kinases (JNK) are activated by various
stimuli, including UV light, interleukin-1, tumor necrosis factor-
(TNF-), and CD28 costimulation. Induction of JNK by TNF-, a
strong apoptosis inducer, implies a possible role of JNK in the
regulation of programmed cell death. Present studies show that lethal
doses of radiation (GR) induced JNK activities at the early phase
of apoptosis in Jurkat T-cells. We demonstrate that JNK1 was activated
by either the T-cell activation signals, anti-CD28 monoclonal antibody
plus phorbol 12-myristate 13-acetate (PMA), or the apoptosis-inducing
treatment, GR; however, the induction patterns were different. In
contrast to the rapid and transient JNK1 activation caused by CD28
signaling plus PMA, GR induced a delayed and persistent JNK1
activation. This implies a distinct regulatory mechanism and specific
function of JNK1 in irradiated cells. The nuclear and cytosolic JNK1
activities were simultaneously increased in the irradiated cells
without an evident change in the protein levels. The abilities of GR to
induce JNK1 activation and DNA fragmentation were correlated.
Peripheral blood lymphocytes were more sensitive to GR than Jurkat
cells in JNK1 induction. The responsiveness of JNK1 to GR suggests the
involvement of JNK1 in the initiation of the apoptosis process.
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