Immunogenic cell death and DAMPs in cancer therapy

Nature reviews. Cancer, Journal Year: 2012, Volume and Issue: 12(12), P. 860 - 875

Published: Nov. 15, 2012

Language: Английский

---

ER-stress-induced transcriptional regulation increases protein synthesis leading to cell death

Nature Cell Biology, Journal Year: 2013, Volume and Issue: 15(5), P. 481 - 490

Published: April 26, 2013

Language: Английский

---

Protein misfolding in the endoplasmic reticulum as a conduit to human disease

Nature, Journal Year: 2016, Volume and Issue: 529(7586), P. 326 - 335

Published: Jan. 1, 2016

Language: Английский

---

The Unfolded Protein Response and Cell Fate Control

Molecular Cell, Journal Year: 2017, Volume and Issue: 69(2), P. 169 - 181

Published: Nov. 5, 2017

Language: Английский

---

Endoplasmic Reticulum Stress and Oxidative Stress in Cell Fate Decision and Human Disease

Antioxidants and Redox Signaling, Journal Year: 2014, Volume and Issue: 21(3), P. 396 - 413

Published: April 6, 2014

Significance: The endoplasmic reticulum (ER) is a specialized organelle for the folding and trafficking of proteins, which highly sensitive to changes in intracellular homeostasis extracellular stimuli. Alterations protein-folding environment cause accumulation misfolded proteins ER that profoundly affect variety cellular signaling processes, including reduction–oxidation (redox) homeostasis, energy production, inflammation, differentiation, apoptosis. unfolded protein response (UPR) collection adaptive pathways evolved resolve misfolding restore an efficient environment. Recent Advances: Production reactive oxygen species (ROS) has been linked stress UPR. ROS play critical role many processes can be produced cytosol several organelles, mitochondria. Studies suggest altered redox sufficient stress, could, turn, induce production Critical Issues: Although oxidative coexist pathologic states, whether how these stresses interact unknown. It also unclear stress. In addition, commit cell apoptotic death contribute various degenerative diseases Future Directions: A greater fundamental understanding mechanisms preserve status will provide new information toward development novel therapeutics human diseases. Antioxid. Redox Signal. 21, 396–413.

Language: Английский

---

Protein O-GlcNAcylation: emerging mechanisms and functions

Nature Reviews Molecular Cell Biology, Journal Year: 2017, Volume and Issue: 18(7), P. 452 - 465

Published: May 10, 2017

Language: Английский

---

UPR, autophagy, and mitochondria crosstalk underlies the ER stress response

Trends in Biochemical Sciences, Journal Year: 2015, Volume and Issue: 40(3), P. 141 - 148

Published: Feb. 2, 2015

Language: Английский

---

The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection

Frontiers in Immunology, Journal Year: 2019, Volume and Issue: 9

Published: Jan. 4, 2019

Apoptosis is a form of cell death by which the body maintains homeostasis internal environment. an initiative process that controlled genes and mainly divided into endogenous pathways (mitochondrial pathway), exogenous (death receptor apoptotic induced endoplasmic reticulum (ER) stress. The imbalance in ER results Under specific conditions, stress can be beneficial to body; however, if protein not restored, prolonged activation unfolded response may initiate via up-regulation C/EBP homologous (CHOP). CHOP plays important role stress-induced apoptosis this review focuses on its multifunctional roles process, as well during microbial infection. We summarize upstream downstream apoptosis. also focus newest discoveries functions CHOP-induced infection, including DNA RNA viruses some species bacteria. Understanding how infection will assist with development antimicrobial therapies.

Language: Английский

---

Cellular adaptation to hypoxia through hypoxia inducible factors and beyond

Nature Reviews Molecular Cell Biology, Journal Year: 2020, Volume and Issue: 21(5), P. 268 - 283

Published: March 6, 2020

Language: Английский

---

Decoding cell death signals in liver inflammation

Journal of Hepatology, Journal Year: 2013, Volume and Issue: 59(3), P. 583 - 594

Published: April 6, 2013

Inflammation can be either beneficial or detrimental to the liver, depending on multiple factors. Mild (i.e., limited in intensity and destined resolve) inflammatory responses have indeed been shown exert consistent hepatoprotective effects, contributing tissue repair promoting re-establishment of homeostasis. Conversely, excessive disproportionate permanent) inflammation may induce a massive loss hepatocytes hence exacerbate severity various hepatic conditions, including ischemia-reperfusion injury, systemic metabolic alterations (e.g., obesity, diabetes, non-alcoholic fatty liver disorders), alcoholic hepatitis, intoxication by xenobiotics infection, de facto being associated with irreversible damage, fibrosis, carcinogenesis. Both liver-resident cells Kupffer cells, stellate sinusoidal endothelial cells) that are recruited response injury monocytes, macrophages, dendritic natural killer emit pro-inflammatory signals – but not cytokines, chemokines, lipid messengers, reactive oxygen species contribute apoptotic necrotic demise hepatocytes. In turn, dying release damage-associated molecular patterns that-upon binding evolutionary conserved pattern recognition receptors-activate innate immune system further stimulate responses, establishing highly hepatotoxic feedforward cycle cell death. this review, we discuss cellular mechanisms account for most deleterious effect at level, is, initiation death among

Language: Английский

---