ER stress-induced cell death mechanisms.

By R. Sano, John Calvin Reed. Biochimica et Biophysica Acta, 2013

1,884 citations recorded by the source corpus.

The endoplasmic-reticulum (ER) stress response constitutes a cellular process that is triggered by a variety of conditions that disturb folding of proteins in the ER. Eukaryotic cells have developed an evolutionarily conserved adaptive mechanism, the unfolded protein response (UPR), which aims to clear unfolded proteins and restore ER homeostasis. In cases where ER stress cannot be reversed, cellular functions deteriorate, often leading to cell death. Accumulating evidence implicates ER stress-induced cellular dysfunction and cell death as major contributors to many diseases, making modulators of ER stress pathways potentially attractive targets for therapeutics discovery. Here, we summarize recent advances in understanding the diversity of molecular mechanisms that govern ER stress signaling in health and disease. This article is part of a Special Section entitled: Cell Death Pathways.

Subfields: Cell Biology, Epidemiology, Geriatrics and Gerontology

View Paper: https://www.semanticscholar.org/paper/c6f907debce76e3f96f626c08a1016965a5d3521

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Citations in the corpus

• Endoplasmic Reticulum Stress and Associated ROS (2016, background): “IRE1α also activates apoptotic signaling kinase-1 (ASK-1), activating downstream factors such as Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK), which enhance apoptosis [15–17].”
• Calcium and ROS: A mutual interplay (2015, background): “Increases in ROS and rapid decreases in Ca2þ concentrations in the ER lumen belong to common features of cellular ER stress and UPR activation (Fig.”
• The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “ATF4 translocates to the nucleus, which increases the expression of CHOP and ATF3.”