Upregulation of an inward rectifying K+ channel can rescue slow Ca2+ oscillations in K(ATP) channel deficient pancreatic islets
Fig 1
The key components of the model.
Green arrows are for stimulatory and red circles are for inhibitory pathways. In the wild-type cells, bursting is paced by metabolic oscillations acting on K(ATP) channels. In the KO cells, genetic disruption of K(ATP) channels leads to increased Kir2.1 current, which now drives bursting.