K(+) channel that conducts voltage-dependent outward rectifying currents upon membrane depolarization. Voltage sensing is coupled to K(+) electrochemical gradient in an 'ion flux gating' mode where outward but not inward ion flow opens the gate. Homo- and heterodimerizes to form functional channels with distinct regulatory and gating properties. In pancreatic islets, conducts K(+) countercurrents for Ca(2+) release from the endoplasmic reticulum (ER) and regulates the frequency and duration of cytosolic Ca(2+) oscillations coupled to secretion of pancreatic hormones. In pancreatic beta cells, drives ER Ca(2+) efflux, which in turn activates Ca(2+)-dependent plasma membrane K(+) slow currents and cytosolic Ca(2+) influx, overall contributing to synchronous cytosolic Ca(2+) oscillations. Limits glucose-induced cytosolic Ca(2+) oscillations coupled to second-phase INS secretion. Contributes to beta cell adaptation to acute inflammation by maintaining normal cytosolic Ca(2+) levels and INS secretion. May regulate beta cell mitochondrial Ca(2+) levels either indirectly via ER Ca(2+) efflux or directly by hyperpolarizing the mitochondrial membrane potential. Limits mitochondrial Ca(2+) oscillations and ATP production involved in glucose homeostasis upon metabolic stress. In pancreatic delta cells, limits Ca(2+)-induced Ca(2+)-release involved in somatostatin secretion and modulates islet paracrine signaling involved in glucagon secretion. Permeable to other monovalent cations such as Rb(+) and Cs(+) 