Results 311 to 320 of about 29,098 (325)
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SMG9 drives ferroptosis by directly inhibiting GPX4 degradation
Biochemical and Biophysical Research Communications, 2021Nonsense-mediated mRNA decay (NMD) is a quality control mechanism that plays an integral role in eliminating abnormal mRNA and corresponding proteins. It is unclear whether the NMD pathway is involved in regulating ferroptosis, which is a type of iron-dependent cell death mainly caused by the inhibition of the antioxidant SLC7A11-GPX4 axis.
Leng Han+7 more
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Role of GPX4 in ferroptosis and its pharmacological implication
Free Radical Biology and Medicine, 2019Ferroptosis is a non-apoptotic form of cell death characterized by iron-dependent lipid peroxidation and metabolic constraints. Dependence on NADPH/H+, polyunsaturated fatty acid metabolism, and the mevalonate and glutaminolysis metabolic pathways have been implicated in this novel form of regulated necrotic cell death.
Tobias Seibt+2 more
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Function and regulation of GPX4 in the development and progression of fibrotic disease
Journal of Cellular Physiology, 2022AbstractFibrosis is a common feature of fibrotic diseases that poses a serious threat to global health due to high morbidity and mortality in developing countries. There exist some chemical compounds and biomolecules associated with the development of fibrosis, including cytokines, hormones, and enzymes.
Zhaobing Li+4 more
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GPX4: The hub of lipid oxidation, ferroptosis, disease and treatment
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, 2023Glutathione peroxidase 4 (GPx4) moonlights as structural protein and antioxidase that powerfully inhibits lipid oxidation. In the past years, it is considered as a key regulator of ferroptosis, which takes role in the lipid and amine acid metabolism and influences the cell aging, oncogenesis, and cell death.
Yi, Liu+4 more
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Redox homeostasis maintained by GPX4 facilitates STING activation
Nature Immunology, 2020Stimulator-of-interferon genes (STING) is vital for sensing cytosolic DNA and initiating innate immune responses against microbial infection and tumors. Redox homeostasis is the balance of oxidative and reducing reactions present in all living systems. Yet, how the intracellular redox state controls STING activation is unclear.
Jan Rehwinkel+20 more
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Mouse Models for Glutathione Peroxidase 4 (GPx4) [PDF]
The selenoperoxidase glutathione peroxidase 4 (GPx4 – also frequently referred to as phospholipid hydroperoxide glutathione peroxidase, PHGPx) is one of the eight glutathione peroxidases in mammals, but the only one known to be essential for early mouse development.
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Targeting GPX4 palmitoylation to boost antitumor immunity
Trends in CancerDespite significant milestones in cancer immunotherapy, tumor cells often escape immune surveillance. Zhou et al. revealed that the pivotal ferroptosis suppressor glutathione peroxidase 4 (GPX4) can undergo palmitoylation by zDHHC8, enhancing ferroptosis resistance.
Daehee Hwang, Whitney S. Henry
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Selenium affects the expression of GPx4 and catalase in the liver of chicken
Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology, 2010A total of 128 chickens (Gallus gallus, broilers) were used to investigate the effect of organic selenium (Se) in expression of catalase (CAT) and phospholipid hydroperoxidase 4 (GPx4) genes. There were 4 replicates of 4 dietary treatments: T1 (basal diet with no added Se), T2 (T1 with 0.15 ppm Se added), T3 (T1 with 0.3 ppm Se) and T4 (T1 with 3.0 ppm
Constantinos A. Georgiou+4 more
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Lipid peroxidation and GPx4: the players of the oxygen paradox
Free Radical Biology and Medicine, 2018Ferroptosis recapitulates the history of oxygen toxicity and lipid peroxidation. Ferroptosis is involved in degenerative diseases and is proposed as a relevant mechanism of onco-suppression. Oxygen, polyunsaturated fatty acids, iron from a labile pool, and seemingly a lipoxygenase are all required for lipid peroxidation that can only take place in the ...
Mattia Zaccarin+11 more
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Unraveling Masked GPX4 Inhibitors
Synfacts, 2020Alexander J. E. Novak, Dirk Trauner
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