Format

Send to

Choose Destination
See comment in PubMed Commons below
Cell. 2007 Aug 10;130(3):563-9.

Does sumoylation control K2P1/TWIK1 background K+ channels?

Author information

  • 1Institut de Pharmacologie Mol├ęculaire et Cellulaire, CNRS UMR6097, Institut Paul Hamel, 660, route des lucioles, 06560 Valbonne, France.

Abstract

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.

PMID:
17693262
DOI:
10.1016/j.cell.2007.06.012
[PubMed - indexed for MEDLINE]
Free full text

LinkOut - more resources

Full Text Sources

Molecular Biology Databases

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center