Key result
The tertiary structure of the C-terminal domain of Kv1.3 is necessary and sufficient for interaction with KCNE4, which causes intracellular retention of the channel.
Population
In vitro models studying the voltage-dependent K+ channel Kv1.3 and KCNE4 subunit in leukocytes
Design
Preclinical
Authors
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May modulate immune cell excitability via Kv1.3 retention; leaves open therapeutic targeting in inflammation.
Identifies the molecular mechanisms by which KCNE4 interacts with and regulates the intracellular retention of Kv1.3 channels in leukocytes.
Solé et al. (2016) studied this question. KCNE4 co-expression vs. Absence of KCNE4 was evaluated on Molecular interaction and intracellular retention of Kv1.3. The tertiary structure of the C-terminal domain of Kv1.3 is necessary and sufficient for interaction with KCNE4, which causes intracellular retention of the channel.
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