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

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Physiological ER Stress: The Model of Insulin-Secreting Pancreatic b-Cellses give rise to a peculiar pattern of acute regulation of the UPR by nutrients. At low non-stimulatory glucose concentrations, when intracellular ATP, [Ca.]. and protein synthesis are low, the IRE1-XBP1 branch of the UPR is at its lowest level of activation while the PERK-eIF2α-ATF4 branch of the UP

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Pathological ER Stress in β Cellsological to pathological UPR and proapoptotic signaling in a variety of environmental and genetic diabetic conditions are addressed. In addition, therapeutic approaches to modulate the level of β cell ER stress and mitigate UPR activation are discussed. Finally, we propose that the identification of

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Cardiovascular Disease and Endoplasmic Reticulum Stress ER-associated degradation (ERAD) of mis-folded proteins. The UPR can also trigger apoptosis if the insult is prolonged or severe. The cardiovascular system has recently been linked to ER stress with an ability to protect the heart, but is also observed to be pathologically damaging. Suppression of

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Book 2012ria cross-talk, the signaling pathways engaged and cellular responses to ER stress, including the adaptive Unfolded Protein Response (UPR), autophagy as well as cell death. Next the book addresses the role of ER stress in physiology and in the etiology of relevant pathological conditions, like carci

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Endoplasmic Reticulum Stress in Health and Disease

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