Expression of multiple KCNE genes in human heart may enable variable modulation of

S38G single-nucleotide polymorphism at the KCNE1 locus is associated with heart failure

“…15,6 Data from experimental studies performed in rabbit and human hearts demonstrated a prolongation of the APD in left ventricular myocytes isolated from failing rabbit ventricles 16 and that KCNE1 gene expression was significantly higher in myocytes from HF patients in comparison with controls, thus contributing to the prolongation of the QT interval through reducing the net outward current during the plateau of the action potential. 6 The KCNE1 gene encodes for a single transmembrane domain protein (minK), which represents the ␤-subunit of a potassium channel able to conduct the slow component (I Ks ) of the delayed-rectifier current, which is relevant in the repolarization of cardiac myocytes.…”

The cardiac I Ks channel, complex indeed

“…In fact, each member of the KCNE family (KCNE1 to -5) has now been shown to interact with KCNQ1, with strikingly different consequences for channel conductance and gating (9). Coassembly with KCNE1 uniquely reproduces the properties of the native I Ks channel by increasing KCNQ1 channel conductance, slowing time course of activation, positively shifting voltagedependent activation, and slowing the time course of deactivation.…”

Protein distribution of Kcnq1, Kcnh2, and Kcne3 potassium channel subunits during mouse embryonic development

“…Coexpression experiments of Kcnq1 and Kcne3 subunits give rise to a constitutively opened pore (Mazhari et al, 2002), whereas coexpression with either Kcne4 or Kcne5 suppresses the current I Ks (Lundquist et al, 2005). Thus, a critical balance of distinct ␤-subunit distribution in relationship with the potassium channel ␣-subunits seems to be compulsory.…”