Abstract
The Na+-Ca2+ exchanger (NCX1) extrudes Ca2+ from cardiac myocytes using the electrochemical gradient of Na+ as a driving force. In addition to being transported, high levels of intracellular Na+ inhibit exchanger current via a process known as Na+-dependent inactivation. To determine its physiological relevance, we introduced the mutation K229Q into the murine NCX1 gene using CRISPR/Cas9. The single site K229Q mutation abolishes the Na+-dependent inactivation process without affecting the other regulatory properties of NCX1 (Matsuoka et al, JPG 109:273-86, 1997).
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