Guards and Culprits in the Endoplasmic Reticulum: Glucolipotoxicity andβ-Cell Failure in Type II Diabetes
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Title
Guards and Culprits in the Endoplasmic Reticulum: Glucolipotoxicity andβ-Cell Failure in Type II Diabetes
Authors
Keywords
-
Journal
Experimental Diabetes Research
Volume 2012, Issue -, Pages 1-9
Publisher
Hindawi Limited
Online
2011-10-03
DOI
10.1155/2012/639762
References
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- Mcl-1 downregulation by pro-inflammatory cytokines and palmitate is an early event contributing to β-cell apoptosis
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- Genistein Induces Pancreatic β-Cell Proliferation through Activation of Multiple Signaling Pathways and Prevents Insulin-Deficient Diabetes in Mice
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- Enhanced Signaling Downstream of Ribonucleic Acid-Activated Protein Kinase-Like Endoplasmic Reticulum Kinase Potentiates Lipotoxic Endoplasmic Reticulum Stress in Human Islets
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- GRP78, but Not Protein-disulfide Isomerase, Partially Reverses Hyperglycemia-induced Inhibition of Insulin Synthesis and Secretion in Pancreatic β-Cells
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