Disease relevance of Kcnh1

• The pooled mouse recombinant phages were used to construct an Eag I end-library [1].

High impact information on Kcnh1

• The biophysical properties of channels from the Eag and Erg subfamilies have been described, and based on their characteristic features and expression patterns, Erg channels have been associated with native currents in the heart [2].
• Like Meag currents, Melk2 currents activate relatively quickly, but they lack the nonsuperimposable Cole-Moore shift characteristic of the Eag subfamily [2].
• Transfer of a small segment of the HERG polypeptide to M-eag, consisting largely of the P region and part of the S6 transmembrane domain, is sufficient to confer rapid inactivation and E-4031 sensitivity to M-eag [3].
• We have investigated the physiological role of the "rapidly activating" delayed rectifier K+ current (IKr) in pacemaker activity in isolated sinoatrial node (SAN) myocytes and the expression of mouse ether-a-go-go (mERG) genes in the adult mouse SAN [4].
• Here, we describe basic properties of Eag and M-EAG channels expressed in frog oocytes, using two-electrode voltage clamp and patch clamp techniques [5].

Biological context of Kcnh1

• Single copy probes derived from CpG-rich island clones from Eag I and Not I linking libraries and nine rare-cutter restriction endonucleases were used to investigate the methylation status of CpG-rich islands on the inactive and active X chromosomes (Chr) of the mouse [6].
• The Eag I end-fragments were subsequently subcloned using a simple procedure taking advantage of the inserted plasmid [1].
• The isolation of evolutionarily conserved Eag I end-clones from mouse chromosome 17 using cloned DNA [1].

References