A new regulation mechanism for KCNN4, the Ca<sup>2+</sup>-dependent K<sup>+</sup> channel, by molecular interactions with the Ca<sup>2+</sup>pump PMCA4b.
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ABSTRACT: KCNN4, a Ca2+-activated K+ channel, is involved in various physiological and pathological processes. It is essential for epithelial transport, immune system, and other physiological mechanisms, but its activation is also involved in cancer pathophysiology as well as red blood cell (RBC) disorders. The activation of KCNN4 in RBC leads to loss of KCl and water, a mechanism known as the "Gardos effect" described 70 years ago. This Ca2+-induced dehydration is irreversible in human RBC and must be tightly controlled to prevent not only hemolysis but also alterations in RBC rheological properties. In this study, we have investigated the regulation of KCNN4 activity after changes in RBC Ca2+ concentration. Using electrophysiology, immunoprecipitation, a
SUBMITTER: Allegrini B
PROVIDER: S-EPMC11787511 | biostudies-literature | 2024 Dec
REPOSITORIES: biostudies-literature
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