Referenced in: none

Automatically associated channels: TASK1

Title: Cell proliferation, potassium channels, polyamines and their interactions: a mini review.

Authors: Thomas M Weiger, Anton Hermann

Journal, date & volume: Amino Acids, 2014 Mar , 46, 681-8

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/23820618

Abstract
Polyamines, which are obligatory molecules involved in cell cycling and proliferation, are subject to a change in their free intracellular concentrations during the cell cycle. Potassium (K(+)) channels are also considered, but less well recognized, to be necessary for cell proliferation by either hyperpolarizing or depolarizing cells during the cell cycle. A block of polyamine synthesis as well as block or knockout of K(+) channels can halt cell proliferation. K(+) channels like BK (maxi calcium (Ca(2+))-activated K(+)), Kir (inward rectifier), M-type K(+)-and TASK (two-pore domain K(+)) channels or the delayed rectifier K(+) channels are modulated in their electrical properties by polyamines. Polyamines are most effective in blocking these channels when applied to the intracellular face of these channels except for TASK channels where they act only from the extracellular side. Quinidine, a general K(+) channel blocker, was found to reduce putrescine concentrations, to block the ornithine decarboxylase and halt cell proliferation. From these results, the question arises if there is an interaction between polyamines, K(+) channels and proliferation. It might be speculated that a decrease of intracellular polyamines allows more K(+) channels to be active, thus inducing hyperpolarization, while an increase of the polyamine concentration may block K(+) channel activity leading to depolarization of the membrane potential. On the other hand, a block or a deletion of K(+) channels may cause a decrease of the polyamine concentration in cells. More research is needed to test these hypotheses.