Cardiac KCNK (K2P) Channel Antibody Explorer Kit

A Screening Package of Cardiac KCNK (K2P) Channel Antibodies Economically Priced
  • Lyophilized Powder
  • Antigen Incl.
Cat #: AK-340
Last update: 24/01/2020

Alomone Labs is pleased to offer the Cardiac KCNK (K2P) Channel Antibody Explorer Kit (#AK-340). This Explorer Kit includes cardiac KCNK channel antibodies with their respective peptide control antigen. An ideal tool for screening purposes.

For research purposes only, not for human use


Product NameCat #Size
Anti-KCNK1 (TWIK-1) (extracellular) Antibody
APC-110 1 x 50 µl
Anti-KCNK3 (TASK-1) Antibody
APC-024 1 x 50 µl
Anti-KCNK4 (TRAAK) Antibody
APC-108 1 x 50 µl
Anti-KCNK6 (TWIK-2) Antibody
APC-040 1 x 50 µl

Scientific Background

Scientific Background
    • K2P channels are involved in various physiological and pathological processes including vascular and pulmonary hypertension, depression and cardiac arrhythmias. 

      K2P channels have two pore domains (P1 and P2) and form dimers thus creating a unit with four pore domains. Each pore domain is bordered by two membrane spanning helices (M1, M2, M3 and M4). The channel’s N- and C- termini are cytoplasmic and there is an extended extracellular loop between P1 and M1. This loop interacts with the same structure of the other subunit of the dimer and it contains a cysteine residue involved in the formation of a covalent bridge between the two subunits1. TWIK1 channels are a subtype of K2P channels that are expressed in the heart and primarily in atrial and purkinje fibers. TWIK1 mediate “background” potassium currents that participate in maintaining resting membrane potential.

      At very low plasma K+ levels hypokalemia can cause severe cardiac arrhythmias leading to sudden death. One of the mechanisms for arrhythmia is a paradoxical depolarization of cardiac myocytes that can initiate the onset of arrhythmia. Recently, it was suggested that TWIK1 channels are involved in this pathological activity by changing ion selectivity and becoming more permeable to Na+ and conducting an inward current of Na+ under hypokalemic conditions. This inward leak is prolonged even after reaching K+ equilibrium and has a substantial effect on membrane resting potential2.

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