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1 ace of Sec was commonly observed in GPx1 and glutathione peroxidase 4.
2 s the lipid hydroperoxide-detoxifying enzyme glutathione peroxidase 4.
3 embrane destruction that can be inhibited by glutathione peroxidase 4.
4 cells independent of RSL3's presumed target, glutathione peroxidase 4.
5 antly down-regulating the antioxidant enzyme glutathione peroxidase-4.
6 ted expression of phospholipid hydroperoxide glutathione peroxidase 4, an enzyme that regulates membr
7 tgrowth requires lipid ROS detoxification by glutathione peroxidase 4 and its cofactor glutathione.
8 elevated levels of the mitochondrial form of glutathione peroxidase 4 and was fully dependent on the
9 strated by decreased expression of catalase, glutathione peroxidase 4, and glutathione synthetase gen
10 letion, the insufficiency of the antioxidant glutathione peroxidase-4, and the hemolysis products hem
11 study, solute carrier family 7 member 11 and glutathione peroxidase 4 are involved in GSH synthesis d
13 to actuate ferroptosis in a fraction of K14+ glutathione peroxidase 4-deficient (Gpx4-deficient) epid
14 d treatment resistance in part by preventing glutathione peroxidase 4-dependent (GPX4-dependent) ferr
16 peroxidation via the activity of the enzyme glutathione peroxidase 4 (GPX-4), is generated directly
17 on of the active center of the selenoprotein glutathione peroxidase 4 (Gpx4(cys/-)) sensitize kidneys
19 to reduction in glutathione (GSH) level and glutathione peroxidase 4 (GPX4) activity, which cause fe
22 educed levels of superoxide dismutase (Sod), glutathione peroxidase 4 (Gpx4) and peroxiredoxin 3 (Prd
23 ine 337 (S337), allowing it to interact with glutathione peroxidase 4 (GPX4) and stabilize the protei
25 ulti-tiered approach consistently identified Glutathione Peroxidase 4 (GPX4) as the top candidate gen
26 donor to trigger symmetric dimethylation of glutathione peroxidase 4 (GPX4) at the conserved arginin
27 have defined the cysteine-glutathione (GSH)-glutathione peroxidase 4 (GPX4) axis as the central defe
28 aled that the pivotal ferroptosis suppressor glutathione peroxidase 4 (GPX4) can undergo palmitoylati
29 (2)O(2)), promoted glutathione depletion and glutathione peroxidase 4 (GPX4) degradation in cardiomyo
30 duced COL2A1 expression, fewer chondrocytes, glutathione peroxidase 4 (GPX4) downregulation, and 4-hy
34 mplex I inhibitors on ferroptosis induced by glutathione peroxidase 4 (GPX4) inhibition is limited.
35 revealed that treatment of cancer cells with glutathione peroxidase 4 (GPX4) inhibitors results in in
46 hat cellular redox homeostasis maintained by glutathione peroxidase 4 (GPX4) is required for STING ac
50 te-specific knockout mice lacking either the glutathione peroxidase 4 (GPx4) or thioredoxin reductase
52 glutathione-dependent lipid hydroperoxidase glutathione peroxidase 4 (GPX4) prevents ferroptosis by
54 s in phospholipids such as that catalyzed by glutathione peroxidase 4 (GPX4) protect cells from ferro
58 sms to suppress ferroptosis: one mediated by glutathione peroxidase 4 (GPX4) that catalyzes the reduc
59 atic niche by shifting their dependency from glutathione peroxidase 4 (GPX4) to ferroptosis suppresso
60 , MceF recruits the host antioxidant protein Glutathione Peroxidase 4 (GPX4) to the mitochondria.
63 andscape, and can be exploited by inhibiting glutathione peroxidase 4 (GPX4) with small-molecules.
65 e phospholipid hydroperoxide-reducing enzyme glutathione peroxidase 4 (GPX4)(3,4) and radical-trappin
67 ments reveal SteviX4 acts as an inhibitor of glutathione peroxidase 4 (GPX4), a critical protein that
68 ll ferroptosis by altering the expression of glutathione peroxidase 4 (GPX4), a crucial antioxidant e
69 mammalian nerve repair, we show that loss of Glutathione peroxidase 4 (GPX4), a crucial suppressor of
70 is inducer that triggered the degradation of glutathione peroxidase 4 (GPX4), a key ferroptosis repre
71 of NFE2L2, by maintaining the expression of glutathione peroxidase 4 (GPX4), a key protein that prev
72 igher levels of phospholipid hydroperoxidase glutathione peroxidase 4 (Gpx4), a major antioxidant enz
74 iredoxin 6 (PRDX6) as a crucial modulator of glutathione peroxidase 4 (GPX4), affecting its localizat
75 ical in lipid radical detoxification through glutathione peroxidase 4 (GPX4), also increases ferropto
77 ct of lipid hydroperoxides, we overexpressed glutathione peroxidase 4 (GPx4), an enzyme that targets
79 membranes unless the lipid hydroperoxidase, glutathione peroxidase 4 (GPX4), reduces these toxic lip
80 dency on the lipid antioxidant selenoenzyme, glutathione peroxidase 4 (GPx4), that acts as a ferropto
81 otein response and antioxidative activity of glutathione peroxidase 4 (GPX4), which are compromised i
82 orm of cell death triggered by inhibition of glutathione peroxidase 4 (GPX4), which catalyzes the red
83 nocysteine-containing enzyme (selenoprotein) glutathione peroxidase 4 (GPX4), which detoxifies lipid
85 f glutathione metabolism pathways, including glutathione peroxidase 4 (GPX4), which protected cells f
94 f the transcriptional repressor CREMa to the glutathione peroxidase 4 (Gpx4, the key ferroptosis regu
95 ependent cell death process, is regulated by glutathione peroxidase-4 (GPX4) and involves lipid perox
96 is infection and an important involvement of glutathione peroxidase-4 (Gpx4) in the necrotic patholog
97 3a2 inhibition was synthetically lethal with glutathione peroxidase-4 (GPX4) inhibition; GPX4 inhibit
99 hibit ferroptosis induced by inactivation of glutathione peroxidase-4 (GPX4) or deletion of the gene
100 iated with reduced levels of glutathione and glutathione peroxidase-4 (Gpx4), along with increased fr
101 ptosis but not in that induced by inhibiting glutathione peroxidase-4 (GPX4), the most downstream com
105 xygenase in concert with low glutathione and glutathione peroxidase 4 levels, DMF induces lipid perox
106 mine, an anticancer drug, as an inhibitor of glutathione peroxidase 4 lipid repair activity, which wa
107 ial superoxide dismutase protein levels, and glutathione peroxidase 4-mediated lipid oxidative damage
108 Moreover, decrease in lipid peroxides by glutathione peroxidase-4 or superoxide by mitochondrial
110 n of lipid peroxidation by overexpression of glutathione peroxidase 4 restored functionalities in CD8
112 including thioredoxin reductases 1 and 3 and glutathione peroxidase 4, were expressed in normal or re