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J. Biol. Chem., Vol. 266, Issue 30, 19938-19944, 10, 1991
MP Peppelenbosch, LG Tertoolen and SW de Laat
The earliest responses to activation of the epidermal growth factor (EGF)
receptor include a transient increase in calcium influx and a transient
membrane hyperpolarization. The underlying mechanisms are, however, not
well understood as yet. In the present study, we have applied patch clamp
recording in the cell-attached and the outside-out mode, and fluorimetric
cytosolic Ca2+ determinations, to identify the nature of the ion channels
involved, to characterize their properties at the level of single channels,
and to unravel their mechanism of activation. We provide evidence that
activation of the EGF receptor results initially in the activation of
voltage-independent Ca2+ channels that can be defined as direct
receptor-operated channels. This in turn causes the activation of
Ca(2+)-dependent K+ channels, which results in a (delayed) membrane
hyperpolarization and then leads to the activation of a second class of
Ca2+ channels that are sensitive to hyperpolarization. An autocatalytic
generation of further hyperpolarization and Ca2+ influx is the predicted
outcome of this ionic cascade. Based on the observed inhibitory effects of
protein kinase C activation on the activity of Ca(2+)-dependent K+
channels, we propose that protein kinase C is involved in the negative
regulation of this cascade, which explains the transient nature of these
responses.
Epidermal growth factor-activated calcium and potassium channels
Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht.
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