The KCNE2 potassium channel β subunit is required for normal lung function and resilience to ischemia and reperfusion injury.

ABSTRACT: The KCNE2 single transmembrane-spanning voltage-gated potassium (K_v) channel β subunit is ubiquitously expressed and essential for normal function of a variety of cell types, often via regulation of the KCNQ1 K_v channel. A polymorphism upstream of KCNE2 is associated with reduced lung function in human populations, but the pulmonary consequences of KCNE2 gene disruption are unknown. Here, germline deletion of mouse Kcne2 reduced pulmonary expression of potassium channel α subunits Kcnq1 and Kcnb1 but did not alter expression of other Kcne genes. Kcne2 colocalized and coimmunoprecipitated with Kcnq1 in mouse lungs, suggesting the formation of pulmonary Kcnq1-Kcne2 potassium channel complexes. Kcne2 deletion reduce

SUBMITTER: Zhou L 

PROVIDER: S-EPMC6704464 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature