The role of KCNQ1-KCNE2 in the thyroid
Using the Kcne2 knockout mouse model that we generated, combined with techniques ranging from positron emission tomography to patch-clamp electrophysiology, we have discovered a crucial role of KCNQ1-KCNE2 channels in the thyroid gland. KCNQ1-KCNE2 is required for normal iodide uptake through the sodium/iodide symporter (NIS), and we found that Kcne2 deletion causes hypothyroidism, especially during gestation, lactation, or old age. Together with our collaborator Nancy Carrasco (Yale University) who cloned NIS, we are continuing to investigate the mechanisms underlying NIS regulation by KCNQ1.