Home > Publications database > PRDX6 contributes to selenocysteine metabolism and ferroptosis resistance. > print |
001 | 294550 | ||
005 | 20241209085543.0 | ||
024 | 7 | _ | |a 10.1016/j.molcel.2024.10.027 |2 doi |
024 | 7 | _ | |a pmid:39547224 |2 pmid |
024 | 7 | _ | |a 1097-2765 |2 ISSN |
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037 | _ | _ | |a DKFZ-2024-02325 |
041 | _ | _ | |a English |
082 | _ | _ | |a 610 |
100 | 1 | _ | |a Chen, Zhiyi |b 0 |
245 | _ | _ | |a PRDX6 contributes to selenocysteine metabolism and ferroptosis resistance. |
260 | _ | _ | |a New York, NY |c 2024 |b Elsevier |
336 | 7 | _ | |a article |2 DRIVER |
336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1733730890_17662 |2 PUB:(DE-HGF) |
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336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
500 | _ | _ | |a DKFZ-ZMBH Alliance / 84(23), pp. 4645–4659.e9 |
520 | _ | _ | |a Selenocysteine (Sec) metabolism is crucial for cellular function and ferroptosis prevention and begins with the uptake of the Sec carrier, selenoprotein P (SELENOP). Following uptake, Sec released from SELENOP is metabolized via selenocysteine lyase (SCLY), producing selenide, a substrate for selenophosphate synthetase 2 (SEPHS2), which provides the essential selenium donor, selenophosphate (H2SePO3-), for the biosynthesis of the Sec-tRNA. Here, we discovered an alternative pathway in Sec metabolism mediated by peroxiredoxin 6 (PRDX6), independent of SCLY. Mechanistically, we demonstrate that PRDX6 can readily react with selenide and interact with SEPHS2, potentially acting as a selenium delivery system. Moreover, we demonstrate the functional significance of this alternative route in human cancer cells, revealing a notable association between elevated expression of PRDX6 and human MYCN-amplified neuroblastoma subtype. Our study sheds light on a previously unrecognized aspect of Sec metabolism and its implications in ferroptosis, offering further possibilities for therapeutic exploitation. |
536 | _ | _ | |a 311 - Zellbiologie und Tumorbiologie (POF4-311) |0 G:(DE-HGF)POF4-311 |c POF4-311 |f POF IV |x 0 |
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650 | _ | 7 | |a cancer metabolism |2 Other |
650 | _ | 7 | |a cell death |2 Other |
650 | _ | 7 | |a ferroptosis |2 Other |
650 | _ | 7 | |a neuroblastoma |2 Other |
650 | _ | 7 | |a selenium |2 Other |
650 | _ | 7 | |a selenocysteine metabolism |2 Other |
700 | 1 | _ | |a Inague, Alex |b 1 |
700 | 1 | _ | |a Kaushal, Kamini |0 P:(DE-He78)3273a29ccb056de5321a084dec4f94c2 |b 2 |u dkfz |
700 | 1 | _ | |a Fazeli, Gholamreza |b 3 |
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700 | 1 | _ | |a Xavier da Silva, Thamara N |b 5 |
700 | 1 | _ | |a Dos Santos, Ancely Ferreira |b 6 |
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700 | 1 | _ | |a Freitas, Florencio Porto |b 8 |
700 | 1 | _ | |a Yildiz, Umut |b 9 |
700 | 1 | _ | |a Viviani, Lucas Gasparello |b 10 |
700 | 1 | _ | |a Lima, Rodrigo Santiago |b 11 |
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700 | 1 | _ | |a Mañas, Adriana |b 21 |
700 | 1 | _ | |a Hondal, Robert |b 22 |
700 | 1 | _ | |a Bartenhagen, Christoph |b 23 |
700 | 1 | _ | |a Fischer, Matthias |b 24 |
700 | 1 | _ | |a Shimada, Briana K |b 25 |
700 | 1 | _ | |a Seale, Lucia A |b 26 |
700 | 1 | _ | |a Chillon, Thilo Samson |b 27 |
700 | 1 | _ | |a Fabiano, Marietta |b 28 |
700 | 1 | _ | |a Schomburg, Lutz |b 29 |
700 | 1 | _ | |a Schweizer, Ulrich |b 30 |
700 | 1 | _ | |a Netto, Luis E |b 31 |
700 | 1 | _ | |a Meotti, Flavia C |b 32 |
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700 | 1 | _ | |a Miyamoto, Sayuri |b 35 |
700 | 1 | _ | |a Friedmann Angeli, José Pedro |b 36 |
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