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10.3390/cells9092066 http://scihub22266oqcxt.onion/10.3390/cells9092066 32927693!7563782!32927693     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32927693&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Cells 2020 ; 9 (9): ? Nephropedia Template TP {{tp|p=32927693|t=2020. ER Stress-Induced Secretion of Proteins and Their Extracellular Functions in the Heart |pdf=|usr=}}{{32927693}} gab.com Text ER Stress-Induced Secretion of Proteins and Their Extracellular Functions in the Heart JO: Cells http://www.kidney.de/pget.php?&tw=1&pmid=32927693 #FOAvip Endoplasmic reticulum (ER) stress is a result of conditions that imbalance protein homeostasis or proteostasis at the ER, for example ischemia, and is a common event in various human pathologies, including the diseased heart. Cardiac integrity and function depend on the active secretion of mature proteins from a variety of cell types in the heart, a process that requires an intact ER environment for efficient protein folding and trafficking to the secretory pathway. As a consequence of ER stress, most protein secretion by the ER secretory pathway is decreased. Strikingly, there is a select group of proteins that are secreted in greater quantities during ER stress. ER stress resulting from the dysregulation of ER Ca(2+) levels, for instance, stimulates the secretion of Ca(2+)-binding ER chaperones, especially GRP78, GRP94, calreticulin, and mesencephalic astrocyte-derived neurotrophic factor (MANF), which play a multitude of roles outside the cell, strongly depending on the cell type and tissue. Here we review current insights in ER stress-induced secretion of proteins, particularly from the heart, and highlight the extracellular functions of these proteins, ranging from the augmentation of cardiac cell viability to the modulation of pro- and anti-apoptotic, oncogenic, and immune-stimulatory cell signaling, cell invasion, extracellular proteostasis, and more. Many of the roles of ER stress-induced protein secretion remain to be explored in the heart. This article is part of a special issue entitled "The Role of Proteostasis Derailment in Cardiac Diseases." Twit Text FOAVip ER Stress-Induced Secretion of Proteins and Their Extracellular Functions in the Heart ????Cells http://www.kidney.de/pget.php?&tw=1&pmid=32927693 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32927693 #FOAvip English Wikipedia <ref>{{Cite pmid|32927693}}</ref> ER Stress-Induced Secretion of Proteins and Their Extracellular Functions in the Heart #MMPMID32927693 Meyer BA; Doroudgar S Cells 2020[Sep]; 9 (9): ? PMID32927693show ga Endoplasmic reticulum (ER) stress is a result of conditions that imbalance protein homeostasis or proteostasis at the ER, for example ischemia, and is a common event in various human pathologies, including the diseased heart. Cardiac integrity and function depend on the active secretion of mature proteins from a variety of cell types in the heart, a process that requires an intact ER environment for efficient protein folding and trafficking to the secretory pathway. As a consequence of ER stress, most protein secretion by the ER secretory pathway is decreased. Strikingly, there is a select group of proteins that are secreted in greater quantities during ER stress. ER stress resulting from the dysregulation of ER Ca(2+) levels, for instance, stimulates the secretion of Ca(2+)-binding ER chaperones, especially GRP78, GRP94, calreticulin, and mesencephalic astrocyte-derived neurotrophic factor (MANF), which play a multitude of roles outside the cell, strongly depending on the cell type and tissue. Here we review current insights in ER stress-induced secretion of proteins, particularly from the heart, and highlight the extracellular functions of these proteins, ranging from the augmentation of cardiac cell viability to the modulation of pro- and anti-apoptotic, oncogenic, and immune-stimulatory cell signaling, cell invasion, extracellular proteostasis, and more. Many of the roles of ER stress-induced protein secretion remain to be explored in the heart. This article is part of a special issue entitled "The Role of Proteostasis Derailment in Cardiac Diseases." |*Endoplasmic Reticulum Stress[MESH] |*Myocardium/cytology/metabolism/pathology[MESH] |Animals[MESH] |Endoplasmic Reticulum Chaperone BiP[MESH] |Heart[MESH] |Heart Diseases/*metabolism/pathology[MESH] |Humans[MESH] |Molecular Chaperones/metabolism[MESH] |Proteostasis[MESH] |Signal Transduction[MESH]ER Stress-Induced Secretion of Proteins and Their Extracellular Functi(epmc).pdf DeepDyve Pubget Overpricing