A Combined “Omics” Approach Identifies N-Myc Interactor as a Novel Cytokine-induced Regulator of IRE1α Protein and c-Jun N-terminal Kinase in Pancreatic Beta Cells (original ) (raw )A combined ″omics″ approach identifies NMI as a novel cytokine-induced regulator of IRE1α and JNK in pancreatic beta cells
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The c-Jun amino-terminal kinase pathway is preferentially activated by interleukin-1 and controls apoptosis in differentiating pancreatic beta-cells
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Arquivos Brasileiros de Endocrinologia & Metabologia, 2008
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Cytokines Downregulate the Sarcoendoplasmic Reticulum Pump Ca2+ ATPase 2b and Deplete Endoplasmic Reticulum Ca2+, Leading to Induction of Endoplasmic Reticulum Stress in Pancreatic β-Cells
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Diabetes, 2005
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Variations in IB1/JIP1 Expression Regulate Susceptibility of β-Cells to Cytokine-Induced Apoptosis Irrespective of C-Jun NH2-Terminal Kinase Signaling
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JNK1 Deficient Insulin-Producing Cells Are Protected against Interleukin-1β-Induced Apoptosis Associated with Abrogated Myc Expression
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Dominant Negative MyD88 Proteins Inhibit Interleukin-1beta /Interferon-gamma -mediated Induction of Nuclear Factor kappa B-dependent Nitrite Production and Apoptosis in beta Cells
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