Titlebook: Endoplasmic Reticulum Stress in Health and Disease; Patrizia Agostinis,Samali Afshin Book 2012 Springer Science+Business Media Dordrecht 2

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Biology of the Endoplasmic Reticulumrly studies focused on the structure, which was then followed by biochemical and functional studies associated with calcium storage and release from the ER, protein folding and secretion, ER associated degradation (ERAD) and ER stress responses. Currently there is a significant interest in the role

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A Tight-Knit Group: Protein Glycosylation, Endoplasmic Reticulum Stress and the Unfolded Protein Resc reticulum (ER), details concerning the interconnected nature of pathways associated with protein glycosylation, ER stress and the unfolded protein response are only now beginning to come to light. Changes in glycosylation may induce ER stress or may be induced by ER stress. It has been established

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Endoplasmic Reticulum-mitochondria connections, calcium cross-talk and cell fate: a closer inspectiohighly interconnected structures that are physically based on the most abundant intracellular membranes: ., those forming the endoplasmic reticulum (ER) and the mitochondrial networks. Main hubs of these infra-structures are the Mitochondria-Associated Membranes (MAMs), ER and mitochondria juxtapose

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ER Stress and UPR Through Dysregulated ER Ca2+ Homeostasis and Signalingre filling is critical for proper protein folding. In many occasions, ER stress is tightly linked to disruption of ER Ca. homeostasis, causing the activation of an integrated signaling pathway, the unfolded protein response (UPR). In this book chapter, we will review the ER as a dynamic intracellula

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Regulation of ER Stress Responses by microRNAsirect posttranscriptional regulation of gene expression, typically by binding to 3’ UTR of cognate mRNAs and inhibiting their translation and/or stability. Hundreds of miRNAs, many of them evolutionarily conserved, have been identified in mammals, but their physiological functions are just beginning

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Pathological ER Stress in β Cellstancy. The reduction in functional β cell mass due to increased β cell apoptosis and decreased β cell proliferation is a crucial factor in the pathogenesis of diabetes mellitus. Mounting clinical and experimental research findings suggest that endoplasmic reticulum (ER) stress and activation of the

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