Key result
Different signaling pathways affect Kv7.1 and KCNE channels through various mechanisms, which could potentially provide novel ways of targeting the channel pharmacologically.
Why the study?
Development of pharmaceuticals targeting Kv7.1 is problematic due to differing pharmacological sensitivity and modulation by KCNE subunits.
Key points are not available for this paper at this time.
Design
Review
Understanding the hormonal signaling pathways affecting Kv7.1 and KCNE channels may provide novel strategies for targeting these channels, which are crucial for cardiac repolarization.
Kv7 channels (Kv7.1–7.5) are voltage-gated K + channels that can be modulated by five β-subunits (KCNE1–5). Kv7.1-KCNE1 channels produce the slow-delayed rectifying K + current, I Ks , which is important during the repolarization phase of the cardiac action potential. Kv7.2–7.5 are predominantly neuronally expressed and constitute the muscarinic M-current and control the resting membrane potential in neurons. Kv7.1 produces drastically different currents as a result of modulation by KCNE subunits. This flexibility allows the Kv7.1 channel to have many roles depending on location and assembly partners. The pharmacological sensitivity of Kv7.1 channels differs from that of Kv7.2–7.5 and is largely dependent upon the number of β-subunits present in the channel complex. As a result, the development of pharmaceuticals targeting Kv7.1 is problematic. This review discusses the roles and the mechanisms by which different signaling pathways affect Kv7.1 and KCNE channels and could potentially provide different ways of targeting the channel.
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Thompson et al. (2020) reported a review. Different signaling pathways affect Kv7.1 and KCNE channels through various mechanisms, which could potentially provide novel ways of targeting the channel pharmacologically.
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