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J. Biol. Chem., Vol. 267, Issue 4, 2123-2126, Feb, 1992
AP Lieberman, PM Pitha and ML Shin
Tumor necrosis factor (TNF) is a pleiotropic biomodulator and an important
inducer of certain pathophysiologic immune reactions such as granuloma
formation, cachexia, and septic shock. The production of TNF by astrocytes,
which may figure prominently in the development of immune responses within
the central nervous system, is subject to post- transcriptional regulation.
We have previously shown that in virus- stimulated astrocytes, inhibition
of protein kinase C results in a specific, 10-fold decrease in TNF mRNA
half-life. Here we show that the decay of TNF messages induced in the
macrophage-like cell line RAW 264.7 by either virus or lipopolysaccharide
was subject to similar regulation, and that this pathway influenced the
amount of TNF protein released by stimulated cells. Using a modified RNase
protection assay, we demonstrate that inhibition of protein kinase C
significantly enhanced the rate of poly(A) removal from TNF mRNA, thus
facilitating an early event in the process of mRNA degradation.
Poly(A) removal is the kinase-regulated step in tumor necrosis factor mRNA decay
Department of Pathology, University of Maryland School of Medicine, Baltimore 21201.
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