Electrostatic interactions during Kv1.2 N-type inactivation: random-walk simulation

Abstract

N-type inactivation of the Kv1.2 voltage-gated potassium channel is a process in which the N-terminal of the protein (its first 20 amino acids) binds to the open-channel surface, extends and occludes its pore. This process has been experimentally studied in both intact and ShBDelta6-46 channels in which the inactivating peptides are supplied in the bath solution. In this work we provide a qualitative description of N-type inactivation by simulating the random walk of charged inactivating peptides in the electrostatic field that originates from the charges present in the channel and in the cellular membrane. Our results give a deeper insight into the previously reported influence of electrostatics on the rate of N-type inactivation of ShBDelta6-46. We also show how the enchaining of the peptides, i.e., considering the intact form of the channel, influences the N-type inactivation with different charges of those peptides.

On the biophysics of cathodal galvanotaxis in rat prostate cancer cells: Poisson–Nernst–Planck equation approach

“…The unbalanced charge sticks to the membrane within the Debye length (Rubinstein 1990), contributing to a gradient in the ionic concentration. The Debye length in a cellular environment is of the order of 0.7 nm (Małysiak and Grzywna 2009), which cannot be directly reflected by the results on a lattice spacing of 1 μm, and a smaller spacing is impossible to apply due to computer time limitations. The boundary concentration change shown in the chart is therefore averaged over 1 μm, and one should bear in mind that it is expected to be 1 μm/0.7 nm = 1,429 times larger within the Debye layer where the concentration can reach a value being 18 % smaller than it is in the bulk concentration.

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