The stability of TNF mRNA in virus-stimulated astrocytes is regulated through a novel, kinase-dependent pathway.
Hypothesis-generating for astrocyte TNF regulation; does not support clinical translation of these kinase inhibitors.
Infection of astrocytes with Newcastle disease virus stimulated the production of 1,2-diacylglycerol, and resulted in the kinase-dependent expression of mRNAs encoding tumor necrosis factor (TNF), interferon alpha and beta, and interleukin 6. The half-life of TNF mRNA was significantly decreased in the presence of protein kinase inhibitors H-7 and staurosporine, but not in the presence of HA1004. In contrast to the decay of TNF mRNA, the half-lives of other cytokine mRNAs were only minimally affected by the kinase inhibitors. These data indicated that the stability of TNF mRNA was regulated through a novel, kinase-dependent pathway.
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Lieberman et al. (1990) studied this question.
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