Does Sumoylation Control K2P1/TWIK1 Background K+ Channels?

نویسندگان

  • Sylvain Feliciangeli
  • Saïd Bendahhou
  • Guillaume Sandoz
  • Pierre Gounon
  • Markus Reichold
  • Richard Warth
  • Michel Lazdunski
  • Jacques Barhanin
  • Florian Lesage
چکیده

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.

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عنوان ژورنال:
  • Cell

دوره 130  شماره 

صفحات  -

تاریخ انتشار 2007