Endoplasmic Reticulum Stress Is Chronically Activated in Chronic Pancreatitis
Raghuwansh P. Sah,Sushil Kumar Garg,Ajay Dixit,Vikas Dudeja,Rajinder K. Dawra,Ashok K. Saluja +5 more
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TLDR
It is established that ER stress is chronically activated in CP and is induced early in pancreatic injury through pathologic calcium signaling independent of trypsinogen activation.About:
This article is published in Journal of Biological Chemistry.The article was published on 2014-10-03 and is currently open access. It has received 85 citations till now. The article focuses on the topics: Trypsinogen activation & Unfolded protein response.read more
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Mitochondrial Dysfunction, Through Impaired Autophagy, Leads to Endoplasmic Reticulum Stress, Deregulated Lipid Metabolism, and Pancreatitis in Animal Models
György Biczó,Eszter T. Vegh,Natalia Shalbueva,Olga A. Mareninova,Jason M. Elperin,Ethan Lotshaw,Sophie Gretler,Aurelia Lugea,Sudarshan R. Malla,David W. Dawson,Piotr Ruchala,Julian P. Whitelegge,Samuel W. French,Li Wen,Sohail Z. Husain,Fred S. Gorelick,Péter Hegyi,Péter Hegyi,Zoltán Rakonczay,Ilya Gukovsky,Anna S. Gukovskaya +20 more
TL;DR: In different animal models, a central role is found for mitochondrial dysfunction, and for impaired autophagy as its principal downstream effector, in development of AP, a model of severe AP the pathogenesis of which has remained unknown.
Journal ArticleDOI
Autophagy, Inflammation, and Immune Dysfunction in the Pathogenesis of Pancreatitis
TL;DR: The roles of autophagy and inflammation in pancreatitis, mechanisms of deregulation, and connections among disordered pathways are discussed, and gaps in knowledge are identified and perspective directions for research are delineated.
Journal ArticleDOI
Basal autophagy maintains pancreatic acinar cell homeostasis and protein synthesis and prevents ER stress.
Laura Antonucci,Johan Bourghardt Fagman,Ju Youn Kim,Jelena Todoric,Ilya Gukovsky,Mason R. Mackey,Mark H. Ellisman,Michael Karin +7 more
TL;DR: Autophagy is identified as an essential homeostatic process that maintains pancreatic acinar cell function by preventing endoplasmic reticulum stress, reactive oxygen species accumulation, and DNA damage, and basal autophagy preserves the high rates of protein synthesis that characterize the exocrine pancreas.
Journal ArticleDOI
Early Intra-Acinar Events in Pathogenesis of Pancreatitis
TL;DR: Multiple parallel mechanisms, including activation of inflammatory cascades, endoplasmic reticulum stress, autophagy, and mitochondrial dysfunction in the acinar cells are now recognized to be important in driving the profound systemic inflammatory response and extensive pancreatic injury seen in acute pancreatitis.
Journal ArticleDOI
FGF21 Is an Exocrine Pancreas Secretagogue
Katie C. Coate,Genaro Hernandez,Curtis A. Thorne,Shengyi Sun,Thao D. V. Le,Kevin Vale,Steven A. Kliewer,David J. Mangelsdorf +7 more
TL;DR: P pancreatic FGF21 is a digestive enzyme secretagogue whose physiologic function is to maintain acinar cell proteostasis through an autocrine/paracrine mechanism that requires signaling through a tyrosine kinase receptor complex composed of an FGF receptor and β-Klotho.
References
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Signal integration in the endoplasmic reticulum unfolded protein response
David Ron,Peter Walter +1 more
TL;DR: Together, at least three mechanistically distinct arms of the UPR regulate the expression of numerous genes that function within the secretory pathway but also affect broad aspects of cell fate and the metabolism of proteins, amino acids and lipids.
Journal ArticleDOI
The Unfolded Protein Response: From Stress Pathway to Homeostatic Regulation
Peter Walter,David Ron +1 more
TL;DR: The vast majority of proteins that a cell secretes or displays on its surface first enter the endoplasmic reticulum, where they fold and assemble, and only properly assembled proteins advance from the ER to the cell surface.
Journal ArticleDOI
XBP1 mRNA Is Induced by ATF6 and Spliced by IRE1 in Response to ER Stress to Produce a Highly Active Transcription Factor
TL;DR: The transcription factor XBP1, a target of ATF6, is identified as a mammalian substrate of such an unconventional mRNA splicing system and it is shown that only the spliced form of X BP1 can activate the UPR efficiently.
Journal ArticleDOI
IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA
Marcella Calfon,Huiqing Zeng,Fumihiko Urano,Jeffery H. Till,Stevan R. Hubbard,Heather P. Harding,Scott G. Clark,David Ron +7 more
TL;DR: It is demonstrated that mutations in either ire-1 or the transcription-factor-encoding xbp-1 gene abolished the UPR in Caenorhabditis elegans, suggesting that physiological ER load regulates a developmental decision in higher eukaryotes.
Journal ArticleDOI
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease
TL;DR: The endoplasmic reticulum is the major site in the cell for protein folding and trafficking and is central to many cellular functions and is emerging as a potential site for the intersection of inflammation and metabolic disease.
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