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

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Vichi, P. et al.

Endothelin- stimulated ERK activation in airway smooth-muscle cells requires calcium influx and Raf activation.

Endothelin (ET)-1 is a 21-amino-acid peptide that is a potent vasoconstrictor and mitogen. By binding to its G-protein coupled receptor, ET-1 stimulates the proliferation of airway smooth-muscle (ASM) cells, which may be involved in the pathogenesis of asthma. The ETB receptor stimulates activation of the extracellular regulated kinase 2 (ERK2), which is thought to be required for proliferation of ASM cells. Our findings reveal that ET rapidly activates Raf, and that dominant-negative Raf interferes with ET- induced ERK activation in ASM cells. Expression of the amino-terminal Ras-binding domain of Raf inhibited ET- induced ERK activation, suggesting that ET-stimulated Raf activation is a Ras-dependent process. Furthermore, ET-stimulated ERK and Raf activation in ASM cells require calcium influx; chelating extracellular calcium or preventing calcium influx through calcium channels inhibited ET-stimulated, but not phorbol ester-stimulated, ERK and Raf activation.[1]

References

Endothelin-stimulated ERK activation in airway smooth-muscle cells requires calcium influx and Raf activation. Vichi, P., Whelchel, A., Knot, H., Nelson, M., Kolch, W., Posada, J. Am. J. Respir. Cell Mol. Biol. (1999) [Pubmed]

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