Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities

By Inki Kim, W. Xu, John Calvin Reed. Nature reviews. Drug discovery, 2008

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How researchers see this paper

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Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy (2017, background): “cell death, and neurotransmitter release, specifically glutamate (38, 39).”
Mechanisms of tau-induced neurodegeneration (2009, neutral): “The chronic accumulation of the hyperphosphorylated tau as a misfolded protein in the ER could cause neurodegeneration due to protracted ER stress [91].”
Tau in Alzheimer Disease and Related Tauopathies (2010, background): “The chronic accumulation of the hyperphosphorylated tau as a misfolded protein in the ER could cause neurodegeneration due to protracted ER stress [93].”
The Role of the PERK/eIF2α/ATF4/CHOP Signaling Pathway in Tumor Progression During Endoplasmic Reticulum Stress (2016, background): “The main aim of activated UPR branches is to rebalance the ER homeostasis, but under severe and prolonged stress conditions the pro-apoptotic arm of UPR is activated and cells undergo apoptosis [101].”
The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “Thus, CHOP expression can be upregulated by XBP1(s) (44) (45) (46) .”