ライフサイエンスコーパス: GPx4

1 cally dependent on glutathione peroxidase 4 (GPX4).

2 t enzymes, such as glutathione peroxidase 4 (GPX4).

3 inked to decreased glutathione peroxidase 4 (GPX4).

4 ses CKB binding to glutathione peroxidase 4 (GPX4).

5 rily controlled by glutathione peroxidase 4 (GPX4).

6 luding antioxidant glutathione peroxidase 4 (GPX4).

7 id hydroperoxidase glutathione peroxidase 4 (GPX4).

8 erozygous expression of catalytically silent Gpx4.

9 from mice specifically lacking mitochondrial Gpx4.

10 y nearly complete reduction in expression of GPX4.

11 electrophilic warheads that bind and inhibit GPX4.

12 ells that are able to complement the loss of GPX4.

13 suggesting a possible link between AURKA and GPX4.

14 kine response of IECs which is restricted by GPX4.

15 tion of reactive groups capable of targeting GPX4.

16 ecame dependent on the ferroptosis inhibitor GPX4.

17 reported to activate the enzyme activity of GPX4.

18 that persister cells acquire a dependency on GPX4.

19 -inhibiting enzyme glutathione peroxidase 4 (GPX4)(10).

20 nocysteine insertion sequence element in the GPX4 3' untranslated region, and the rare allele of this

21 de-reducing enzyme glutathione peroxidase 4 (GPX4)(3,4) and radical-trapping antioxidants(5,6).

22 Glutathione peroxidase 4 (GPX4)(5,6) and ferroptosis suppressor protein 1 (FSP1)(7

23 show that loss of Glutathione peroxidase 4 (GPX4), a crucial suppressor of ferroptosis, promotes fun

24 cules that inhibit glutathione peroxidase 4 (GPX4), a phospholipid peroxidase, cause lethal accumulat

25 on the phospholipid glutathione peroxidase (GPX4), a selenocysteine-containing enzyme that dissipate

26 spinal motor neuron degeneration induced by Gpx4 ablation exhibited features of ferroptosis, includi

27 neuron degeneration and paralysis induced by Gpx4 ablation suggest that ferroptosis inhibition by GPX

28 d in ferroptosis of motor neurons induced by Gpx4 ablation.

29 the onset of paralysis and death induced by Gpx4 ablation.

30 ic site in GPX4 and successfully found eight GPX4 activators using a novel computational strategy and

31 Meanwhile, the discovery of GPX4 activators verified the possibility of rational des

32 Cs) in Crohn's disease (CD) exhibit impaired GPX4 activity and signs of LPO.

33 The strongest compound, 1d4, increased GPX4 activity to 150% at 20 muM in the cell-free assay a

34 Compound 1 from the virtual screen increased GPX4 activity, suppressed ferroptosis, reduced pro-infla

35 ues showed reduced glutathione peroxidase 4 (GPx4) activity (p < 0.05) and iron accumulation, indicat

36 of glutathione and glutathione peroxidase-4 (Gpx4), along with increased free iron, mitochondrial sup

37 cient animals, the resulting males (Sec46Ala-Gpx4(+/-)+Alox15(-/-)) showed normalized fertility, and

38 xification through glutathione peroxidase 4 (GPX4), also increases ferroptosis.

39 Glutathione peroxidase 4 (GPX4), an antioxidant defense enzyme active in repairing

40 he impact of high-iron diets or depletion of Gpx4, an antioxidant enzyme reported as an important fer

41 Gpx4, an enzyme that protects against PUFA-mediated lipi

42 We also detected a remarkable decrease in GPX4, an inhibitor of ferroptosis, with an increase in c

43 dation accumulation, along with key protein (GPX4 and ACSL4) expression alteration during reperfusion

44 ally, the diabetes-induced downregulation of GPx4 and antioxidant Nrf2 in pancreatic tissue was signi

45 related genes, MnSOD, CuZnSOD, Nrf2, Keap1, GPx4 and Catalase was also examined.

46 ding inhibition of the lipid hydroperoxidase GPX4 and detachment from the extracellular matrix, induc

47 lone parallel system, which co-operates with GPX4 and glutathione to suppress phospholipid peroxidati

48 In summary, we found elevated expression of GPX4 and higher sensitivity to ferroptosis in ACCs.

49 through pan-selenoprotein inhibition beyond GPX4 and identifies ALKBH8, a tRNA-selenocysteine methyl

50 A or reconstitution of miR-4715-3p inhibited GPX4 and induced cell death, suggesting a link between A

51 l redox homeostasis (decreased levels of GSH/GPX4 and NADP(H), increased reactive oxygen species (ROS

52 Pharmacological selenium (Se) augments GPX4 and other genes in this transcriptional program, th

53 ownregulate the essential antioxidant enzyme GPX4 and stimulate ferroptosis, which is a crucial drive

54 we identified a potential allosteric site in GPX4 and successfully found eight GPX4 activators using

55 le we created heterozygous animals (Sec46Ala-Gpx4(+/-)) and crossed them with Alox15 knock-out mice (

56 Glutathione peroxidase 4 (GPX4) and arachidonic acid 15-lipoxygenase (ALOX15) are

57 s, is regulated by glutathione peroxidase-4 (GPX4) and involves lipid peroxidation markers like malon

58 e dismutase (Sod), glutathione peroxidase 4 (Gpx4) and peroxiredoxin 3 (Prdx3) that render them susce

59 sorbent assay (ELISA) quantified HIF-1alpha, GPX4, and MDA levels.

60 ause homozygous Gpx4 knock-in mice (Sec46Ala-Gpx4(+/+)) are not viable we created heterozygous animal

61 Consistent with the role of GPX4 as a ferroptosis inhibitor, spinal motor neuron deg

62 Our study suggests targeting GPX4 as a therapeutic opportunity in CCCs, and highlight

63 s and ferroptosis modulate sensitivity, with GPX4 as the top sensitiser in both screens.

64 Glutathione peroxidase 4 (GPX4), as the only enzyme in mammals capable of reducing

65 c dimethylation of glutathione peroxidase 4 (GPX4) at the conserved arginine 152 (R152) residue, alon

66 p15 and the glutathione peroxidases GPx1 and GPx4 being substantially reduced.

67 ozoa depends on the moonlighting function of Gpx4 both as an enzyme oxidizing capsular protein thiols

68 ther found that ferroptosis inducers inhibit GPX4 by covalently targeting the active site selenocyste

69 Despite the marked downregulation of GPX4 by HCMV, further inhibition of GPX4 impaired virus

70 and total GPx activity, while knock-down of GPx4 by small interfering RNA (siRNA) increased VEGF, an

71 obal enrichment of selenoproteins, including GPX4, by NRF2 downregulation, and targeting NRF2 and GPX

72 Therefore, we demonstrated that GPX4 can be directly activated using chemical compounds

73 Together, TGR and GPx4 can serve as a novel disulfide bond formation syste

74 ated with ferroptosis and that inhibition of GPX4 causes ferroptotic injury in primary human trophobl

75 s masked nitrile oxide prodrugs that inhibit GPX4 covalently with unique cellular and biochemical rea

76 gy, causing OTUD5 degradation and subsequent GPX4 decay.

77 GPX4 deficiency enhanced cellular lipid peroxidation and

78 itamin K2 can prevent ferroptosis induced by Gpx4 deficiency in iNKT cells and ameliorate the impaire

79 Concordantly, GPX4 deficiency inhibited herpes simplex virus-1 (HSV-1)

80 px4 is essential for mouse survival and that Gpx4 deficiency makes cells vulnerable to oxidative inju

81 might counteract male infertility related to GPX4 deficiency.

82 , ROS accumulation and lipid peroxidation in Gpx4-deficient cells remain high.

83 al T cell responses by using T cell-specific Gpx4-deficient mice.

84 Ex vivo, Gpx4-deficient T cells rapidly accumulated membrane lipi

85 GPx4 deletion reduces keratinocyte adhesion in culture a

86 s protection against ferroptosis elicited by GPX4 deletion.

87 ical Se supplementation effectively inhibits GPX4-dependent ferroptotic death as well as cell death i

88 We find that either high-iron diets or Gpx4 depletion promotes 8-OHG release and thus activates

89 GPX4 detoxifies membrane phospholipid hydroperoxides, th

90 tissues investigated, and overexpression of Gpx4 did not cause alterations in activities of glutathi

91 While GPX4 does not control AA metabolism, cytokine production

92 cells and CD8+ T cells was needed to sustain GPX4 downregulation over time, resulting in ferroptotic

93 ewer chondrocytes, glutathione peroxidase 4 (GPX4) downregulation, and 4-hydroxynonenal (4-HNE) upreg

94 d pharmacological evidence, we conclude that GPX4 dysfunction hypersensitizes mice to ATN during AKI.

95 S died at the same embryonic stage (E7.5) as Gpx4(-/-) embryos as expected.

96 tightly controlled expression of functional Gpx4 emerges as a key for full male fertility.

97 ent during tumor promotion increased hepatic GPx4 expression and reduced the expression of VEGF and o

98 Selenium enhanced GPx4 expression and total GPx activity, while knock-down

99 ely infected mice is associated with reduced Gpx4 expression as well as increased lipid peroxidation

100 fected mice increased glutathione levels and Gpx4 expression that inhibit lipid peroxidation.

101 to undergo ferroptosis because they sustain GPX4 expression, despite their increase in ACSL4.

102 delivered into the brain drives antioxidant GPX4 expression, protects neurons, and improves behavior

103 e STING DNA-sensing pathway, suggesting that GPX4 facilitates STING activation by maintaining redox h

104 n-specific CD8(+) and CD4(+) T cells lacking Gpx4 failed to expand and to protect from acute lymphocy

105 ally, we demonstrate the indispensability of GPX4 for LSC development and the initiation/maintenance

106 Here, we investigated the importance of Gpx4 for physiological T cell responses by using T cell-

107 ) for proliferation and the lipid peroxidase GPX4 for protection from ferroptosis of inner, matrix-de

108 ltered glutathione metabolism that depend on GPX4 for survival and are highly susceptible to ferropto

109 e are dependent on the lipid hydroperoxidase GPX4 for survival.

110 These studies unveil an essential role of Gpx4 for T cell immunity.

111 d players in ferroptosis regulation, such as GPX4, FSP1, SLC7A11 and ACSL4, discussing frequent pitfa

112 Loss of GPX4 function results in selective persister cell ferrop

113 ptotic responses without apparent effects on GPX4 function.

114 ncoding antioxidant enzymes, including GLRX, GPX4, G6PD, and SEC14L4 (Golgi-transport protein).

115 Notably, depletion of the Gpx4 gene in the memory phase of viral infection did not

116 thal phenotype of null mutation of the mouse Gpx4 gene, indicating that the transgene can replace the

117 de at the N terminus, are generated from the Gpx4 gene.

118 ) using a genomic clone containing the human GPX4 gene.

119 , we generated transgenic mice using mutated GPX4 genes encoding either the long form Gpx4 (lGPX4 gen

120 GPX4 genetic knockdown mirrored RSL3 effect on mTOR path

121 tae, with decreased glutathione content, and GPx4 (glutathione peroxidase 4) expression and activity.

122 ial showed that SNPs can affect responses of GPx4, GPx1 and GPx3 protein expression or activity in re

123 utation of the active site selenocysteine of Gpx4 (Gpx4_U46S).

124 dative damage repair (CAT, SOD1, SOD2, GPX1, GPX4, GSR, TXN, TXN2, TXNRD1, and TXNRD2) and survival i

125 tion of common variants in SOD1, SOD2, GPX1, GPX4, GSR, TXNRD1, and TXN2.

126 significantly lower including PRX1 and PRX3, GPX4, GSTP1, GCLC, and MTHFD2.

127 Endothelium-specific deletion of Gpx4 had no obvious impact on normal vascular homeostasi

128 e 152 (R152) residue, along with a prolonged GPX4 half-life.

129 GPX4 has emerged as a promising therapeutic target for c

130 nduction of ferroptosis by the inhibition of GPX4 has emerged as a therapeutic strategy to trigger ca

131 ccompanied with upregulated protein level of GPX4, HMOX1 and SOD1 and their enzymatic activities.

132 ounds that inhibit glutathione peroxidase 4 (GPX4) hold promise as cancer therapeutics in their abili

133 Additionally, PSAT1-mediated GPX4 hydroxylation correlates with poor immunotherapy ou

134 ation of GPX4 by HCMV, further inhibition of GPX4 impaired virus replication.

135 eroxides in membranes, and overexpression of GPx4 improves mitochondrial respiration and reduces hydr

136 Yet a role of Gpx4 in endothelial cell function has remained enigmatic

137 Direct inhibition of GPX4 in H295R cells led to high necrotic populations com

138 We show that mice with deletion of Gpx4 in hematopoietic cells develop anemia and that Gpx4

139 ic enteritis in mice that lack one allele of Gpx4 in IECs.

140 gene can replace the essential role of mouse Gpx4 in mouse development.

141 Conditional ablation of Gpx4 in neurons of adult mice resulted in rapid onset an

142 er, our findings reveal the critical role of Gpx4 in regulating iNKT cell homeostasis and function, t

143 The expression of glutathione peroxidase 4 (GPX4) in H295R cells, however, is significantly higher w

144 of phospholipid hydroperoxide-specific GPx (GPx4) in NIH/3T3 cells led to increases in cellular pero

145 Mechanistically, GPX4 inactivation increased production of lipid peroxida

146 Depletion or inhibition of GPX4 increases sensitivity to palbociclib and giredestra

147 ed by excitotoxicity or ER stress, which are GPX4 independent.

148 Recent data have revealed glutathione/GPX4-independent axes for suppressing ferroptosis, and i

149 hanistic elucidation of structurally diverse GPX4-inhibiting molecules have uncovered novel electroph

150 GPX4 inhibition activated ferroptosis, inducing TC cell

151 HCMV-infected cells became less sensitive to GPX4 inhibition as infection progressed, requiring subst

152 sely, ACSL4 is required for ferroptosis upon GPX4 inhibition but dispensable for p53-mediated ferropt

153 iting this induced collateral sensitivity by GPX4 inhibition clears drug-tolerant populations and lea

154 y acid, in mitigating ferroptosis induced by GPX4 inhibition in vitro or by hypoxia/reoxygenation inj

155 glutathione peroxidase-4 (GPX4) inhibition; GPX4 inhibition is a known trigger of ferroptosis that b

156 eration and the pharmacological mechanism of GPX4 inhibition that generates ROS in lipid environments

157 cient to reduce sensitivity to pharmacologic GPX4 inhibition.

158 e the impaired function of iNKT cells due to Gpx4 inhibition.

159 ls are resistant to ferroptosis triggered by GPX4 inhibition.

160 optosis induced by glutathione peroxidase 4 (GPX4) inhibition is limited.

161 ically lethal with glutathione peroxidase-4 (GPX4) inhibition; GPX4 inhibition is a known trigger of

162 bination treatment with SEMA3C-319aa and the GPX4 inhibitor RSL3 was more effective than monotherapy

163 ing the need to identify factors that govern GPX4 inhibitor sensitivity.

164 Consequently, GPX4 inhibitor treatment selectively induced ferroptotic

165 Although most GPX4 inhibitors rely on a chloroacetamide moiety to modi

166 we show that treatment of cancer cells with GPX4 inhibitors results in acute depletion of N-carbamoy

167 ed, requiring substantially higher levels of GPX4 inhibitors to induce ferroptosis compared to uninfe

168 l targeting of FSP1 strongly synergizes with GPX4 inhibitors to trigger ferroptosis in a number of ca

169 However, sensitivity to GPX4 inhibitors varies greatly across cancer cell lines(

170 d underwent ferroptosis after treatment with GPX4 inhibitors.

171 l reactivity compared to existing classes of GPX4 inhibitors.

172 nsable for ferroptosis induced by erastin or GPX4 inhibitors; conversely, ACSL4 is required for ferro

173 selenium-dependent glutathione peroxidase 4 (GPX4) inhibits ferroptosis, converting unstable ferropto

174 GPX4 is also a prognostic marker in patients with PDAC.

175 Thus, GPX4 is an essential regulator of ferroptotic cancer cel

176 for the hypothesis that common variation in GPX4 is associated with prognosis after a diagnosis of b

177 a chemoproteomics strategy to discover that GPX4 is directly inhibited by a second class of compound

178 The selenoenzyme Gpx4 is essential for early embryogenesis and cell viabi

179 ation suggest that ferroptosis inhibition by GPX4 is essential for motor neuron health and survival i

180 Here we show that GPX4 is essential for motor neuron health and survival i

181 Our previous studies showed that Gpx4 is essential for mouse survival and that Gpx4 defic

182 hematopoietic cells develop anemia and that Gpx4 is essential for preventing receptor-interacting pr

183 is sufficient to trigger ferroptosis because GPX4 is suppressed.

184 The enzyme glutathione peroxidase 4 (GPX4) is a central regulator of ferroptosis, and protect

185 Glutathione peroxidase 4 (Gpx4) is a key enzyme in suppressing ferroptosis by redu

186 antioxidant enzyme glutathione peroxidase 4 (Gpx4) is a key regulator of oxidative stress-induced cel

187 The selenoenzyme glutathione peroxidase 4 (Gpx4) is a major scavenger of phospholipid hydroperoxide

188 Glutathione peroxidase 4 (GPX4) is a selenoenzyme that uses GSH as a co-factor to

189 Glutathione peroxidase-4 (Gpx4) is an enzyme that plays a critical role in prevent

190 Glutathione peroxidase 4 (Gpx4) is an essential antioxidant enzyme having multiple

191 The selenoenzyme glutathione peroxidase 4 (Gpx4) is an intracellular antioxidant enzyme important f

192 Glutathione peroxidase 4 (GPx4) is crucial in the regulation of ferroptosis by con

193 Glutathione peroxidase 4 (GPX4) is essential for cell membrane repair, inflammatio

194 asis maintained by glutathione peroxidase 4 (GPX4) is required for STING activation.

195 Glutathione peroxidase 4 (GPX4) is the guardian of ferroptosis, although its membr

196 Glutathione peroxidase 4 (Gpx4) is uniquely involved in the detoxification of oxid

197 NRF2 downregulation, and targeting NRF2 and GPX4 killed spheroids overall.

198 Because homozygous Gpx4 knock-in mice (Sec46Ala-Gpx4(+/+)) are not viable w

199 To address this question we employed Gpx4 knock-in mice expressing the Sec46Ala-Gpx4 mutant,

200 and mitochondrial reactive oxygen species in Gpx4 knockout iNKT cells.

201 t, aortic explants from endothelium-specific Gpx4 knockout mice showed a markedly reduced number of e

202 upregulated in the skin and keratinocytes of GPx4-knockout mice.

203 Absence of Gpx4 leads to functional inactivation of caspase 8 by gl

204 ciency or dysfunction of a selenoperoxidase, GPX4, leads to ferroptosis.

205 erarchical selenoprotein regulatory program, GPX4 levels are strongly reduced due to impaired transla

206 GPX4 levels were elevated in PM compared to PH (p = 0.03

207 oxidation and increasing the glutathione and GPX4 levels.

208 ted GPX4 genes encoding either the long form Gpx4 (lGPX4 gene) or the short form Gpx4 (sGPX4 gene).

209 a normal phenotype in resting skin, whereas GPx4 loss in the epidermis caused epidermal hyperplasia,

210 GPX4 may be a useful target for drug development, highli

211 These findings suggest that targeting of GPX4 may represent a therapeutic strategy to prevent acq

212 er, QD394 causes an iron- and ROS-dependent, GPX4 mediated cell death, suggesting ferroptosis as a ma

213 1(G93A) mice, both male and female SOD1(G93A)GPX4 mice had extended lifespans.

214 lizes the reduced fertility of male Sec46Ala-Gpx4(+/-) mice by improving the motility of their sperm.

215 When Sec46Ala-Gpx4(+/-) mice were crossed with Alox15-deficient animal

216 Male Sec46Ala-Gpx4(+/-) mice, but not their female littermates, were s

217 less in murine embryonic fibroblasts from Tg(GPX4) mice compared with wild type mice.

218 s of transgenic mice overexpressing Gpx4 (Tg(GPX4) mice) using a genomic clone containing the human G

219 diquat-induced apoptosis was decreased in Tg(GPX4) mice, as evidenced by attenuated caspase-3 activat

220 Both lines of Tg-(GPX4) mice, Tg5 and Tg6, had elevated levels of Gpx4 (mR

221 d by diquat were reduced significantly in Tg(GPX4) mice.

222 there were no differences in total levels of GPX4 mRNA across genotypes.

223 4) mice, Tg5 and Tg6, had elevated levels of Gpx4 (mRNA and protein) in all tissues investigated, and

224 d Gpx4 knock-in mice expressing the Sec46Ala-Gpx4 mutant, in which the catalytic selenocysteine was r

225 ported anti-oxidant gene signature including Gpx4, Nqo1, and Gsta4; common targets of the NF-kB trans

226 mbination, in ER+ breast cancer models, with GPX4 null xenografts being highly sensitive to palbocicl

227 Interestingly, the male Gpx4-null mice rescued by the sGPX4 gene were infertile

228 In Gpx4-null mice rescued by the sGPX4 gene, the Gpx4 prote

229 to rescue the lethal phenotype of the mouse Gpx4-null mutation.

230 to rescue the lethal phenotype of the mouse Gpx4-null mutation.

231 one peroxidase family (GPX1, GPX2, GPX3, and GPX4), one or more iodothyronine deiodinases and two thi

232 data, combining pharmacologic inhibition of GPX4 or SLC7A11 with inhibition of FSP1 demonstrates syn

233 via inhibition of glutathione peroxidase 4 (GPX4) or SLC7A11.

234 lacking either the glutathione peroxidase 4 (GPx4) or thioredoxin reductase 1 (TR1) gene were generat

235 The direct inhibition of GPX4, or indirect inhibition by depletion of its substra

236 Ectopic GPx4 overcame this, reduced peroxidized phospholipid acc

237 GPx4 overexpression also prevented loss of muscle contra

238 GPX4 overexpression and knockdown modulated the lethalit

239 GPx4 overexpression in Sod1KO mice rescued the deficits

240 GPx4 overexpression in Sod1KO mice rescues the impaired

241 and dependent on the FZD7-beta-catenin-Tp63-GPX4 pathway for survival.

242 parallel to the canonical glutathione-based GPX4 pathway.

243 GPX4 perturbation additionally sensitises triple negativ

244 the sperm, including glutathione peroxidase GPx4/PHGPx.

245 These data demonstrate that Gpx4 plays a role in vivo in the mechanism of apoptosis

246 Glutathione peroxidase 4 (GPx4) plays a fundamental role in the reduction of lipid

247 nhibition of the catalytic selenocysteine in Gpx4 prevents elimination of PUFA hydroperoxides; these

248 id hydroperoxidase glutathione peroxidase 4 (GPX4) prevents ferroptosis by converting lipid hydropero

249 Glutathione peroxidase 4 (GPX4) protects against lipid peroxidation (LPO) and cell

250 A long form Gpx4 protein and a short form Gpx4 protein, which are di

251 genic mice with the sGPX4 gene had increased Gpx4 protein in all tissues and were protected against d

252 submitochondrial distribution pattern of the Gpx4 protein in these mice was identical to that in wild

253 nst apoptosis in mice, whereas the long form Gpx4 protein is important for male fertility.

254 rated for the first time that the short form Gpx4 protein is present in somatic tissue mitochondria a

255 genic mice with the lGPX4 gene had increased Gpx4 protein only in the testes, and the lGPX4 gene fail

256 As a selenoprotein, GPX4 protein synthesis is highly inefficient and energet

257 px4-null mice rescued by the sGPX4 gene, the Gpx4 protein was present in mitochondria isolated from s

258 A long form Gpx4 protein and a short form Gpx4 protein, which are distinguishable by the presence

259 targets, the most prominent among them being GPX4 protein.

260 ound between the total amounts of HIF-1a and GPX4 (r = 0.460, p < 0.01).

261 tion of all selenoproteins, mice ablated for GPx4 recovered after 5 weeks and had a normal life span.

262 d hydroperoxidase, glutathione peroxidase 4 (GPX4), reduces these toxic lipid species.

263 l carcinomas are particularly susceptible to GPX4-regulated ferroptosis.

264 Although Gpx4 represents a key component of the reactive oxygen s

265 GPX4 represents a promising yet difficult-to-drug therap

266 droperoxide glutathione peroxidase (PHGPX or GPX4), respectively.

267 udy identifies dietary PUFAs as a trigger of GPX4-restricted mucosal inflammation phenocopying aspect

268 rol uptake-addicted lymphoma cells abolishes GPX4, resulting in cancer cell death by a mechanism cons

269 GPX4 rs713041 is located near the selenocysteine inserti

270 wo single nucleotide polymorphisms (SNPs) in GPX4 (rs713041 and rs757229) were associated with all-ca

271 GPX4's role in oxidative stress regulation, its potentia

272 PD), and defense against lipid peroxidation (GPX4) scored high as synthetic sick/lethal.

273 enoprotein gene expression, in particular in GPx4, SelK, SelM, SelW, and Sep15.

274 An efficacy study in mouse using a GPX4-sensitive tumor model found that doses of 24 up to

275 m both enzymes are apparently expressed, and GPX4 serves as anti-oxidative enzyme but also as a struc

276 ong form Gpx4 (lGPX4 gene) or the short form Gpx4 (sGPX4 gene).

277 GPx4 silencing led to 2-4-fold increases in PG-G formati

278 Conversely, GPx4 siRNA knockdown enhanced phospholipid peroxidation,

279 by the expression of the key markers such as GPx4, SLC7A11, NRF2, and HO1.

280 ow for the first time that in the absence of Gpx4, sufficient vitamin E supplementation is crucial fo

281 Glutathione peroxidase 4 (GPX4) suppresses ferroptosis by reducing lipid hydropero

282 GPX4 suppression in tumor cells can induce ferroptosis.

283 two lines of transgenic mice overexpressing Gpx4 (Tg(GPX4) mice) using a genomic clone containing th

284 uced by inhibiting glutathione peroxidase-4 (GPX4), the most downstream component of the ferroptosis

285 These data link the activity of cutaneous GPx4 to the regulation of COX-2 and hair follicle morpho

286 teins involved in antioxidant defense (Gpx1, Gpx4, TR1, SelS, SelK, and Sps2).

287 The human GPX4 transgene rescued the lethal phenotype of null muta

288 Five selenoproteins (Gpx4, Txnrd1, Txnrd2, Dio3, and Sepp1) were classified a

289 GPX4 upregulation provides unique drug discovery opportu

290 Glutathione peroxidase 4 (GPX4) uses glutathione to protect cells from ferroptosis

291 Glutathione peroxidase 4 (GPX4) utilizes glutathione (GSH) to detoxify lipid perox

292 Dependency on GPX4 was found to exist across diverse therapy-resistant

293 Recently, the cytosolic form of Gpx4 was identified as an upstream regulator of a novel

294 t for 6 weeks before endothelial deletion of Gpx4 was induced by 4-hydroxytamoxifen.

295 ptosis, whereas the mitochondrial isoform of Gpx4 was previously shown to be crucial for male fertili

296 d by inhibition of glutathione peroxidase 4 (GPX4), which catalyzes the reduction of lipid peroxides

297 on was mediated by glutathione peroxidase 4 (GPx4), which preferentially degrades lipid peroxides.

298 athways, including glutathione peroxidase 4 (GPX4), which protected cells from chemotherapy-induced o

299 Glutathione peroxidase-4 (GPx4), which specifically metabolizes lipid hydroperoxid

300 ited by inhibiting glutathione peroxidase 4 (GPX4) with small-molecules.