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- W934851696 abstract "The aim of the present investigation was to delineate cytokine-induced signaling and death using the EndoC-βH1 cells as a model for primary human beta-cells. The cytokines IL-1β and IFN-γ induced a rapid and transient activation of NF-κB, STAT-1, ERK, JNK and eIF-2α signaling. The EndoC-βH1 cells died rapidly when exposed to IL-1β + IFN-γ, and this occurred also in the presence of the actinomycin D. Inhibition of NF-κB and STAT-1 did not protect against cell death, nor did the cytokines activate iNOS expression. Instead, cytokines promoted a rapid decrease in EndoC-βH1 cell respiration and ATP levels, and we observed protection by the AMPK activator AICAR against cytokine-induced cell death. It is concluded that EndoC-βH1 cell death can be prevented by AMPK activation, which suggests a role for ATP depletion in cytokine-induced human beta-cell death." @default.
- W934851696 created "2016-06-24" @default.
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- W934851696 date "2015-10-01" @default.
- W934851696 modified "2023-10-14" @default.
- W934851696 title "Role of the AMP kinase in cytokine-induced human EndoC-βH1 cell death" @default.
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- W934851696 doi "https://doi.org/10.1016/j.mce.2015.07.015" @default.
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