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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Activation of the sphingomyelin signaling pathway in intact EL4 cells and in a cell-free system by IL-1 beta.

The mechanism of interleukin-1 (IL-1) signaling is unknown. Tumor necrosis factor-alpha uses a signal transduction pathway that involves sphingomyelin hydrolysis to ceramide and stimulation of a ceramide-activated protein kinase. In intact EL4 thymoma cells, IL-1 beta similarly stimulated a rapid decrease of sphingomyelin and an elevation of ceramide, and enhanced ceramide-activated protein kinase activity. This cascade was also activated by IL-1 beta in a cell-free system, demonstrating tight coupling to the receptor. Exogenous sphingomyelinase, but not phospholipases A2, C, or D, in combination with phorbol ester replaced IL-1 beta to stimulate IL-2 secretion. Thus, IL-1 beta signals through the sphingomyelin pathway.[1]

References

  1. Activation of the sphingomyelin signaling pathway in intact EL4 cells and in a cell-free system by IL-1 beta. Mathias, S., Younes, A., Kan, C.C., Orlow, I., Joseph, C., Kolesnick, R.N. Science (1993) [Pubmed]
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