Key result
KCNQ1 antagonist C293B impairs thyroid I(-) uptake ~68%, indicating KCNQ1-KCNE2 is required for NIS activity.
Why the study?
The mechanistic role of the KCNQ1-KCNE2 potassium channel in thyroid hormone biosynthesis and iodide uptake was not fully understood.
Does KCNQ1-KCNE2 channel disruption impair thyroid I- uptake in mice?
Does KCNQ1-KCNE2 channel disruption impair thyroid I- uptake in mice?
Absolute Event Rate: 0.009% vs 0.028%
The KCNQ1-KCNE2 potassium channel is required for adequate thyroid cell I- uptake, providing a mechanistic explanation for hypothyroidism and resulting cardiac hypertrophy in genetic disruption models.
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KCNQ1-KCNE2 disruption may impair thyroid iodide uptake in mice; leaves open relevance to human hypothyroidism or cardiac hypertrophy.
Purtell et al. (2012) studied Hypothyroidism. KCNQ1-specific antagonist (-)-[3R,4S]-chromanol 293B (C293B) vs. Vehicle was evaluated on Thyroid cell I(-) uptake (dSUV/dt). The KCNQ1-specific antagonist C293B significantly impaired thyroid cell I(-) uptake in vivo (0.009 vs 0.028 min-1) and in vitro, indicating KCNQ1-KCNE2 is required for adequate NIS activity.
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