Does sumoylation control K2P1/TWIK1 background K+ channels?

Sylvain Feliciangeli (1) , Saïd Bendahhou (1) , Guillaume Sandoz (1) , Pierre Gounon (2) , Markus Reichold (3) , Richard Warth (3) , Michel Lazdunski (1) , Jacques Barhanin (1) , Florian Lesage (1)

1 IPMC - Institut de pharmacologie moléculaire et cellulaire
2 CCMA - Centre Commun de Microscopie Appliquée
3 Institute of Physiology

A novel model for the regulation of cell excitability has recently been proposed. It originates from the observation that the background K(+) channel K2P1 (TWIK1) may be silenced by sumoylation in Xenopus oocytes and that inactivation of the putative sumoylation site (mutation K274E) gives rise to robust current expression in transfected COS-7 cells. Here, we show that only the mutation K274E, and not K274R, is associated with an increase of K2P1 current density, suggesting a charge effect of K274E. Furthermore, we failed to observe any band shift by western blot analysis that would confirm an eventual sumoylation of K2P1 in COS-7 cells and oocytes.

Domaines: Biochimie, Biologie Moléculaire; Génétique; Biologie animale

Sylvain Feliciangeli, Saïd Bendahhou, Guillaume Sandoz, Pierre Gounon, Markus Reichold, et al.. Does sumoylation control K2P1/TWIK1 background K+ channels?. Cell, 2007, 130 (3), pp.563-9. ⟨10.1016/j.cell.2007.06.012⟩. ⟨hal-00171463⟩