Activation is followed by membrane hyperpolarization, which promotes calcium influx.

This causes sodium channels to accommodate calcium influx into the cell which also results in depolarization.

In a further study, Menerba was shown to regulate calcium influx, which is related to temperature regulation.

Once the two meet, a calcium influx occurs, causing a signaling cascade.

On the molecular level, calcium influx is not the only factor responsible for apoptosis induced by excitoxicity.

This presynaptic event is caused by calcium influx.

Finally it may act by inhibiting calcium influx.

To make muscle contraction possible, a calcium influx from the extracellular fluid into the cell is crucial.

T1 has the original signaling cascade that is involved in the regulation of cell morphology and calcium influx.

Synapsin I was shown to be phosphorylated by this calcium influx.