Alomone Labs is pleased to offer the Cardiac Kir Channel Antibody Explorer Kit (#AK-330). This Explorer Kit includes Cardiac Kir Channel antibodies with their respective peptide control antigen. An ideal tool for screening purposes.
|Product Name||Cat #||Size|
|APC-026||1 x 50 µl|
|BLP-PC026||1 x 40 µg|
|APC-026-GP (formerly AGP-044)||1 x 50 µl|
|BLP-PC026||1 x 40 µg|
|APC-042||1 x 50 µl|
|BLP-PC042||1 x 40 µg|
|APC-005||1 x 50 µl|
|BLP-PC005||1 x 0.12 mg|
|ALM-031||1 x 25 µg|
|APC-027||1 x 50 µl|
|BLP-PC027||1 x 40 µg|
|APC-020||1 x 50 µl|
|BLP-PC020||1 x 40 µg|
Inwardly rectifying potassium channels (Kir) are found in a variety of cells including neurons, blood cells, endothelial cells and myocytes.
Kir channels are comprised of four subunits and each unit divided into a transmembrane and a cytoplasmic domain. The NH2 and COOH domains are located inside the cytosol and are arranged in a tetramer that leads to an extended pore for ion permeation and is mainly responsible for gating regulation. The transmembrane domain is mainly responsible for ion selectivity and gating. It is comprised of outer (TM1) and inner (TM2) membrane spanning helices with two additional short helical elements. The pore is walled by one TM2 helix from each of the four Kir subunits. The channel has two gating mechanisms- slow gating and fast gating.
Kir channels are widely expressed in cardiac myocytes including ventricular and atrial tissue, Purkinje fibers but not nodal cells.
Conductance through the Kir channel (named the Ik1 current) dominates the resting conductance of these cells and is defined as time-independent background K+ current. The channel exhibits a large inward current at the Em more negative than Ek and a relatively large outward current at the Em slightly more positive than Ek. This feature is essential to stabilize the Eres of cardiac myocytes near Ek. However, due to inward rectification, as the membrane is further depolarized the Ik1 current progressively decreases. The lack of outward conductance through Ik1 at positive potentials prevents K+ efflux during the action potential plateau, resulting in the maintenance of depolarization and prolonged cardiac muscle contraction1.
- Hibino, H. et al. (2010) Physiol. Rev. 90, 291.