8.A.10.2.1
K⁺ voltage-gated channel subfamily E member 2 (KCNE2) or minimum K⁺ channel-related peptide (MinK; MiRP1) (β-subunit) [associates with KCNH2/ERG1 and KCNQ1/KVLQT1 (McCrossan et al. 2009), as well as KCNQ2 and KCNQ3] (Eldstrom and Fedida, 2011; Roepke et al., 2006). Regulated by PKCδ phosphorylation (O'Mahony et al., 2007).  A mutation (hERG T473P) in the transmembrane non-pore region  causes clinical manifestations of long QT syndrome (Liu et al. 2012).  Exhibits an array of functions in the heart, stomach, thyroid and choroid plexus. A variety of interconnected disease manifestations caused by KCNE2 disruption involve both excitable cells such as cardiomyocytes, and non-excitable, polarized epithelia (Abbott 2015).  It's secondary structure has been determined (Abbott et al. 2008). Deletion of the Kcne2 structural gene in mice and humans gives rise to impaired insulin secretion as well as type 2 diabetes mellitus (Lee et al. 2017).  The KCNE2 beta subunit is required for normal lung function and resilience to ischemia and reperfusion injury (Zhou et al. 2019).