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Blood, Vol. 93 No. 11 (June 1), 1999:
pp. 3694-3702
Interleukin-4 Synergizes With Raf-1 to Promote Long-Term
Proliferation and Activation of c-jun N-terminal Kinase
Megan K. Levings,
Darrell C. Bessette, and
John W. Schrader
From The Biomedical Research Centre, University of British Columbia,
Vancouver, British Columbia, Canada.
This report shows that interleukin-4 (IL-4), which plays a key role
in regulating immune responses, fails to support cellular growth. We
investigated whether this failure of IL-4 to promote growth was because
of its unique inability to activate the Ras/Raf/Erk pathway. Consistent
with other reports, expression in Ba/F3, a factor-dependent
hematopoietic cell line, of either activated Q61KN-Ras or a
hormone-inducible activated Raf-1, resulted in suppression of apoptosis
but not in long-term growth. However, in the presence of IL-4, Ba/F3
cells that expressed either Q61KN-Ras or activated Raf-1
grew continuously at a rate comparable with that stimulated by IL-3.
Investigation of the biochemical events associated with the stimulation
of long-term growth showed that, as expected, the presence of activated
Raf-1 resulted in an increased activity of extracellular signal
regulated kinase (ERK) mitogen-activated protein kinase
(MAPK) but not of c-jun N-terminal kinase/stress-activated
protein kinase (JNK). However, surprisingly, if IL-4 was present, cells
expressing active Raf-1 exhibited increases in JNK activity. These
observations point to a novel mechanism for JNK activation involving
synergy between Raf-1 and pathways activated by IL-4 and suggest that
in hematopoietic cells proliferation is correlated not only with
"mitogen activated" ERK activity, but also with JNK activity.
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