Why the study?
The mediators responsible for ERK activation resulting from increased intracellular Ca2+ due to membrane depolarization in PC12 cells were not fully understood.
Population
PC12 cell line
Comparison
Membrane depolarization with or without calmodulin inhibitor W13
Design
Preclinical experimental study
Key result
Calmodulin mediates ERK activation induced by increases in intracellular Ca2+ concentration in PC12 cells following membrane depolarization, independent of Trk A and EGFR activation.
Authors
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Calmodulin-ERK signaling in depolarized PC12 cells is hypothesis-generating; leaves open relevance to cardiovascular models or therapies.
In PC12 cells, calmodulin mediates ERK activation induced by membrane depolarization and subsequent calcium influx, independent of Trk A and EGFR activation.
Egea et al. (1998) studied this question. Membrane depolarization and W13 (calmodulin inhibitor) was evaluated on ERK activation. Calmodulin mediates ERK activation induced by increases in intracellular Ca2+ concentration in PC12 cells following membrane depolarization, independent of Trk A and EGFR activation.
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