Article
The MODY-associated KCNK16 L114P mutation increases islet glucagon secretion and limits insulin secretion resulting in transient neonatal diabetes and glucose dyshomeostasis in adults.
eLife - 3 May 2024
Nakhe Arya Y, Dadi Prasanna K, Kim Jinsun, Dickerson Matthew T, Behera Soma, Dobson Jordyn R, Shrestha Shristi, Cartailler Jean-Philippe, Sampson Leesa, Magnuson Mark A, Jacobson David A
Abstract excerpt
The gain-of-function mutation in the TALK-1 K+ channel (p.L114P) is associated with maturity-onset diabetes of the young (MODY). TALK-1 is a key regulator of β-cell electrical activity and glucose-stimulated insulin secretion. The KCNK16 gene encoding TALK-1 is the most abundant and β-cell-restricted K+ channel transcript. To investigate the impact of KCNK16 L114P on glucose homeostasis and confirm its...
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