期刊
CYTOKINE
卷 12, 期 12, 页码 1784-1787出版社
W B SAUNDERS CO
DOI: 10.1006/cyto.2000.0784
关键词
anisomycin; lipopolysaccharide; mitogen-activated protein kinase; p38; protein kinase C
Monocytic THP-1 cells expressed tumour necrosis factor-alpha (TNF-alpha) mRNA, but hardly any detectable TNF-alpha protein and a partially activated MAP kinase ERK-2 in the unstimulated state. Stimulation with phorbol ester led to expression of TNF-alpha protein without significant changes in mRNA, a response that was sensitive to the MEK-1/2 inhibitors PD98059 and U0126. A calcium signal also led to expression of TNF-alpha protein, but now accompanied by a rapid increase in mRNA, A synergistic effect between phorbol ester and calcium ionophore was evident at the level of TNF-alpha protein, but not its mRNA. Stimulation with anisomycin led to a TNF-alpha expression that was sensitive to the p38 inhibitor SB203580, Actinomycin D lowered TNF-alpha mRNA in a similar way as PD98059 but was less inhibitory on PMA- or anisomycin-induced formation of TNF-alpha, thus confirming that these agents acted by causing translational derepression, Thus, in THP-1 cells MAP kinase pathways involving MEK-1/2 and possibly ERK-2 as well as the human p38 analogue mere essential for basal TNF-a mRNA expression and translational activation. (C) 2000 Academic Press.
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