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Forschungsdatenbank PMU-SQQUID

The H+/K+ ATPase Inhibitor SCH-28080 Inhibits Insulin Secretion and Induces Cell Death in INS-1E Rat Insulinoma Cells.
Jakab, M; Ketterl, N; Fürst, J; Beyreis, M; Kittl, M; Kiesslich, T; Hauser-Kronberger, C; Gaisberger, M; Ritter, M;
Cell Physiol Biochem. 2017; 43(3):1037-1051
Originalarbeiten (Zeitschrift)


Beyreis Marlena
Gaisberger Martin
Jakab Martin
Ketterl Nina
Kiesslich Tobias
Kittl Michael
Kronberger Cornelia
Ritter Markus


Glucose-stimulated insulin secretion (GSIS) of pancreatic β-cells involves glucose uptake and metabolism, closure of KATP channels and depolarization of the cell membrane potential (Vmem), activation of voltage-activated Ca2+ currents (ICav) and influx of Ca2+, which eventually triggers hormone exocytosis. Beside this classical pathway, KATP-independent mechanisms such as changes in intracellular pH (pHi) or cell volume, which also affect β-cell viability, can elicit or modify insulin release. In β-cells the regulation of pHi is mainly accomplished by Na+/H+ exchangers (NHEs). To investigate if other proton extrusion mechanisms than NHEs are involved in pH regulation, we tested for the presence of the non-gastric H+/K+ ATPase in rat insulinoma cells and assessed effects of the H+/K+ ATPase inhibitor SCH-28080 on insulin secretion, cell viability and apoptosis.

Find related publications in this database (Keywords)

H+/K+ ATPase
INS-1E cells
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