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Effects of iron-depletion on cell cycle progression in normal human T
lymphocytes: selective inhibition of the appearance of the cyclin A-
associated component of the p33cdk2 kinase
JJ Lucas, A Szepesi, J Domenico, K Takase, A Tordai, N Terada and EW Gelfand
Department of Pediatrics, National Jewish Center for Immunology and
Respiratory Medicine, Denver, CO 80206, USA.
Iron removal by the chelating-agent deferoxamine (DFO) arrests cell cycle
progression of activated human T cells in late G1 phase, before the G1/S
border. The effects of the drug on molecules that regulate progression
through the cell cycle were defined. DFO (10 mumol/L) inhibited induction
of transcription of the cdc2 gene, but had no effect on accumulation of
cdk2, cdk4, or interleukin (IL)-2- transcripts. No detectable p34cdc2
protein accumulated, but synthesis of the p33cdk2 protein was begun. It
accumulated to normal levels during the first 20 to 30 hours of incubation
in the presence of DFO. Furthermore, p33cdk2 was activated as an H1 histone
kinase. As active p33cdk2 primarily represents complexes of the p33 protein
with cyclin E or cyclin A, the effects of DFO on these cyclins were
examined. Although the induction of synthesis and early accumulation of
cyclin E and cyclin E-associated kinase activity appeared normal, the
appearance of cyclin A and cyclin A-associated kinase activity were
inhibited by DFO. However, the production of cyclin A mRNA appeared to be
normal in the presence of DFO. A major effect of DFO in blocking cell cycle
progression may be mediated through inhibition of the appearance of cyclin
A protein and, therefore, a major component of p33cdk2 activity. The
results also indicate that the p33cdk2/cyclin E activity produced in the
presence of DFO was not sufficient for completion of the G1 phase of the
cell cycle.
Volume 86,
Issue 6,
pp. 2268-2280,
09/15/1995
Copyright © 1995 by The American Society of Hematology
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