scholarly journals Fluoride Induces Endoplasmic Reticulum Stress and Inhibits Protein Synthesis and Secretion

2008 ◽  
Vol 116 (9) ◽  
pp. 1142-1146 ◽  
Author(s):  
Ramaswamy Sharma ◽  
Masahiro Tsuchiya ◽  
John D. Bartlett
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Synthesis ◽  
Endoplasmic Reticulum Stress

scholarly journals Autophagy inhibition by biotin elicits endoplasmic reticulum stress to differentially regulate adipocyte lipid and protein synthesis

2019 ◽  
Vol 24 (2) ◽  
pp. 343-350 ◽  
Author(s):  
Senthilraja Selvam ◽  
Anand Ramaian Santhaseela ◽  
Dhasarathan Ganesan ◽  
Sudarshana Rajasekaran ◽  
Tamilselvan Jayavelu
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Synthesis ◽  
Endoplasmic Reticulum Stress ◽  
Autophagy Inhibition

scholarly journals Inhibition of Golgi Apparatus Glycosylation Causes Endoplasmic Reticulum Stress and Decreased Protein Synthesis

2010 ◽  
Vol 285 (32) ◽  
pp. 24600-24608 ◽  
Author(s):  
Yu-Xin Xu ◽  
Li Liu ◽  
Carolina E. Caffaro ◽  
Carlos B. Hirschberg
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Synthesis ◽  
Golgi Apparatus ◽  
Endoplasmic Reticulum Stress

scholarly journals Expression of Endoplasmic Reticulum Chaperones in Cardiac Development

2008 ◽  
Vol 2 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Sylvia Papp ◽  
Xiaochu Zhang ◽  
Eva Szabo ◽  
Marek Michalak ◽  
Michal Opas
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Synthesis ◽  
Embryonic Development ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Cardiac Development ◽  
Large Protein ◽  
Induce Endoplasmic Reticulum Stress ◽  
Caspase 7

To determine if cardiogenesis causes endoplasmic reticulum stress, we examined chaperone expression. Many cardiac pathologies cause activation of the fetal gene program, and we asked the reverse: could activation of the fetal gene program during development induce endoplasmic reticulum stress/chaperones? We found stress related chaperones were more abundant in embryonic compared to adult hearts, indicating endoplasmic reticulum stress during normal cardiac development. To determine the degree of stress, we investigated endoplasmic reticulum stress pathways during cardiogenesis. We detected higher levels of ATF6α, caspase 7 and 12 in adult hearts. Thus, during embryonic development, there is large protein synthetic load but there is no endoplasmic reticulum stress. In adult hearts, chaperones are less abundant but there are increased levels of ATF6α and ER stress-activated caspases. Thus, protein synthesis during embryonic development does not seem to be as intense a stress as is required for apoptosis that is found during postnatal remodelling.

scholarly journals The Role of the Effects of Endoplasmic Reticulum Stress on NLRP3 Inflammasome in Diabetes

2021 ◽  
Vol 9 ◽  
Author(s):  
Shuangyu Lv ◽  
Xiaotian Li ◽  
Honggang Wang
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Synthesis ◽  
Endoplasmic Reticulum Stress ◽  
Nlrp3 Inflammasome ◽  
Basic Research ◽  
Misfolded Proteins ◽  
Pyrin Domain ◽  
Receptor Family ◽  
Oligomerization Domain

Endoplasmic reticulum (ER) is an important organelle for the protein synthesis, modification, folding, assembly, and the transport of new peptide chains. When the folding ability of ER proteins is impaired, the accumulation of unfolded or misfolded proteins in ER leads to endoplasmic reticulum stress (ERS). The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome, can induce the maturation and secretion of interleukin-1beta (IL-1β) and IL-18 through activating caspase-1. It is associated with many diseases. Studies have shown that ERS can regulate NLRP3 inflammasome in many diseases including diabetes. However, the mechanism of the effects of ERS on NLRP3 inflammasome in diabetes has not been fully understood. This review summarizes the recent researches about the effects of ERS on NLRP3 inflammasome and the related mechanism in diabetes to provide ideas for the relevant basic research in the future.

Increased autophagy reduces endoplasmic reticulum stress after neonatal hypoxia–ischemia: Role of protein synthesis and autophagic pathways

2014 ◽  
Vol 255 ◽  
pp. 103-112 ◽  
Author(s):  
Silvia Carloni ◽  
Maria Cristina Albertini ◽  
Luca Galluzzi ◽  
Giuseppe Buonocore ◽  
Fabrizio Proietti ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Synthesis ◽  
Endoplasmic Reticulum Stress ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia
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