Pathophysiological Consequences of KATP Channel Overactivity and Pharmacological Response to Glibenclamide in Skeletal Muscle of a Murine Model of Cantù Syndrome

• Ngā kaituhi matua: Rosa Scala (Author), Fatima Maqoud (Author), Nicola Zizzo (Author), Antonietta Mele (Author), Giulia Maria Camerino (Author), Francesco Alfredo Zito (Author), Girolamo Ranieri (Author), Conor McClenaghan (Author), Theresa M. Harter (Author), Colin G. Nichols (Author), Domenico Tricarico (Author)
• Hōputu: Pukapuka
• I whakaputaina: Frontiers Media S.A., 2020-11-01T00:00:00Z.
• Ngā marau: article
• Urunga tuihono: Connect to this object online.

Cantù syndrome (CS) arises from mutations in ABCC9 and KCNJ8 genes that lead to gain of function (GOF) of ATP-sensitive potassium (KATP) channels containing SUR2A and Kir6.1 subunits, respectively, of KATP channels. Pathological consequences of CS have been reported for cardiac and smooth muscle cel...