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000139754 0247_ $$2doi$$a10.1016/j.cell.2017.11.048
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000139754 037__ $$aDZNE-2020-06076
000139754 041__ $$aEnglish
000139754 082__ $$a610
000139754 1001_ $$aIngold, Irina$$b0
000139754 245__ $$aSelenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis.
000139754 260__ $$aNew York, NY$$bElsevier$$c2018
000139754 264_1 $$2Crossref$$3print$$bElsevier BV$$c2018-01-01
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000139754 520__ $$aSelenoproteins are rare proteins among all kingdoms of life containing the 21st amino acid, selenocysteine. Selenocysteine resembles cysteine, differing only by the substitution of selenium for sulfur. Yet the actual advantage of selenolate- versus thiolate-based catalysis has remained enigmatic, as most of the known selenoproteins also exist as cysteine-containing homologs. Here, we demonstrate that selenolate-based catalysis of the essential mammalian selenoprotein GPX4 is unexpectedly dispensable for normal embryogenesis. Yet the survival of a specific type of interneurons emerges to exclusively depend on selenocysteine-containing GPX4, thereby preventing fatal epileptic seizures. Mechanistically, selenocysteine utilization by GPX4 confers exquisite resistance to irreversible overoxidation as cells expressing a cysteine variant are highly sensitive toward peroxide-induced ferroptosis. Remarkably, concomitant deletion of all selenoproteins in Gpx4cys/cys cells revealed that selenoproteins are dispensable for cell viability provided partial GPX4 activity is retained. Conclusively, 200 years after its discovery, a specific and indispensable role for selenium is provided.
000139754 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000139754 542__ $$2Crossref$$i2018-01-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
000139754 542__ $$2Crossref$$i2019-01-25$$uhttp://www.elsevier.com/open-access/userlicense/1.0/
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000139754 650_7 $$0BBX060AN9V$$2NLM Chemicals$$aHydrogen Peroxide
000139754 650_7 $$0EC 1.11.1.12$$2NLM Chemicals$$aPhospholipid Hydroperoxide Glutathione Peroxidase
000139754 650_7 $$0EC 1.11.1.9$$2NLM Chemicals$$aGlutathione Peroxidase
000139754 650_7 $$0EC 1.11.1.9$$2NLM Chemicals$$aglutathione peroxidase 4, mouse
000139754 650_7 $$0H6241UJ22B$$2NLM Chemicals$$aSelenium
000139754 650_2 $$2MeSH$$aAnimals
000139754 650_2 $$2MeSH$$aApoptosis
000139754 650_2 $$2MeSH$$aCell Survival
000139754 650_2 $$2MeSH$$aCells, Cultured
000139754 650_2 $$2MeSH$$aFemale
000139754 650_2 $$2MeSH$$aGlutathione Peroxidase: genetics
000139754 650_2 $$2MeSH$$aGlutathione Peroxidase: metabolism
000139754 650_2 $$2MeSH$$aHEK293 Cells
000139754 650_2 $$2MeSH$$aHumans
000139754 650_2 $$2MeSH$$aHydrogen Peroxide: toxicity
000139754 650_2 $$2MeSH$$aInterneurons: metabolism
000139754 650_2 $$2MeSH$$aLipid Peroxidation
000139754 650_2 $$2MeSH$$aMale
000139754 650_2 $$2MeSH$$aMice
000139754 650_2 $$2MeSH$$aMice, Inbred C57BL
000139754 650_2 $$2MeSH$$aPhospholipid Hydroperoxide Glutathione Peroxidase
000139754 650_2 $$2MeSH$$aSeizures: etiology
000139754 650_2 $$2MeSH$$aSeizures: metabolism
000139754 650_2 $$2MeSH$$aSelenium: metabolism
000139754 7001_ $$aBerndt, Carsten$$b1
000139754 7001_ $$aSchmitt, Sabine$$b2
000139754 7001_ $$aDoll, Sebastian$$b3
000139754 7001_ $$aPoschmann, Gereon$$b4
000139754 7001_ $$aBuday, Katalin$$b5
000139754 7001_ $$aRoveri, Antonella$$b6
000139754 7001_ $$aPeng, Xiaoxiao$$b7
000139754 7001_ $$aPorto Freitas, Florencio$$b8
000139754 7001_ $$aSeibt, Tobias$$b9
000139754 7001_ $$aMehr, Lisa$$b10
000139754 7001_ $$aAichler, Michaela$$b11
000139754 7001_ $$aWalch, Axel$$b12
000139754 7001_ $$aLamp, Daniel$$b13
000139754 7001_ $$aJastroch, Martin$$b14
000139754 7001_ $$aMiyamoto, Sayuri$$b15
000139754 7001_ $$0P:(DE-2719)2000028$$aWurst, Wolfgang$$b16$$udzne
000139754 7001_ $$aUrsini, Fulvio$$b17
000139754 7001_ $$aArnér, Elias S J$$b18
000139754 7001_ $$aFradejas-Villar, Noelia$$b19
000139754 7001_ $$aSchweizer, Ulrich$$b20
000139754 7001_ $$aZischka, Hans$$b21
000139754 7001_ $$aFriedmann Angeli, José Pedro$$b22
000139754 7001_ $$0P:(DE-HGF)0$$aConrad, Marcus$$b23$$eCorresponding author
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000139754 773__ $$0PERI:(DE-600)2001951-8$$a10.1016/j.cell.2017.11.048$$gVol. 172, no. 3, p. 409 - 422.e21$$n3$$p409-422.e21$$q172:3<409 - 422.e21$$tCell$$v172$$x0092-8674$$y2018
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000139754 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2000028$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b16$$kDZNE
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