The Endoplasmic Reticulum: Folding, Calcium Homeostasis, Signaling, and Redox Control
By A. Görlach, Peter Klappa, Dr. Thomas Kietzmann. Antioxidants and Redox Signaling, 2006
630 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/8bf69d5cbc724a69ee6c0460921ca44e2261e721
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In Cell Biology
- J. Malhotra
- R. Kaufman
- U. Förstermann
- G. Hotamışlıgil
- D. Ron
- C. Hetz
- Laurie H. Glimcher
- Kezhong Zhang
In Molecular Biology
Citations in the corpus
- Vascular oxidative stress, nitric oxide and atherosclerosis. (2014, background): “opening and closing of disulfide bonds to reach the desired thermodynamically struct u es, is a RO source by itself [11].”
- Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, neutral): “The superoxide anion radical Both ER stress and oxidative stress, through ROS generation, may increase leak of Ca 2 (cid:2) from the ER lumen (6, 38, 79).”
- The endoplasmic reticulum and the unfolded protein response. (2007, background): “Both ER stress and oxidative stress, through ROS generation, can increase leak of Ca2+ from the ER lumen [101-103].”
- Redox compartmentalization in eukaryotic cells. (2008, background): “Thus, ER contains both oxidative and reductive mechanisms which allow dynamic control of redox state in association with processing and secretory functions [197].”
- Reactive Oxygen Species in Inflammation and Tissue Injury (2014, neutral): “A related issue is the compartmentalized nature of ROS production that is not easily accessible to antioxidants (146, 213).”
- Pathophysiology of sleep apnea. (2010, background): “However, when this stress is insurmountable, the ER may take on the role of executioner, activating proapoptotic proteins, including CHOP/ GADD153 and caspase-7 (199, 632).”
- METHAMPHETAMINE TOXICITY AND MESSENGERS OF DEATH (2009, background): “In addition to regulating synthesis, folding, and transport of proteins, ER also constitutes the main intracellular store for Ca2+, whose excess can contribute to cell death (Gorlach et al., 2006).”