K+ channels play a central role in determining resting membrane potential and cellular excitability. There is growing recognition that the channels exist not as independent units but as macromolecular complexes able to integrate a plethora of cellular signals to fine-tune channel activities. Interaction of K+ channels with accessory proteins and subunits is increasingly reported as providing mechanisms for channels to respond to a variety of stimuli beyond just changes in membrane potential. One such association is that between some voltage-gated K+ channels and the proteins encoded by the KCNE family of genes. The significance of these interactions is manifest in reports of genetic disorders such as the Long QT Syndrome linked to KCNE mutations and proarrhythmic drug susceptibilities from KCNE polymorphisms. The mechanism by which KCNE-encoded proteins control channel behavior is an emerging story. This article reviews some of the recent work addressing the prototypical KCNE-channel interaction between minK and KvLQT1 (Trends Cardiovascular Med 2002;12:182-187).
|Original language||English (US)|
|Number of pages||6|
|Journal||Trends in Cardiovascular Medicine|
|State||Published - 2002|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine