Redox regulation of metabolic and signaling pathways by thioredoxin and glutaredoxin in NOS-3 overexpressing hepatoblastoma cells
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- 作者：Raú ; l Gonzá ; leza ; b ; raulangello@hotmail.com" class="auth_mail" title="E-mail the corresponding author ; M. José ; Ló ; pez-Gruesoa ; Jordi Muntané ; c ; d ; J. Antonio Bá ; rcenaa ; b ; C. Alicia Padillaa ; b
- 关键词：ACO ; aconitase ; ASK1 ; apoptosis signal-regulating kinase 1 ; Bcl-2 ; B-cell lymphoma 2 ; CaM ; calmodulin ; CD95 ; cluster of differentiation 95 ; DTNB ; 5 ; 5-dithio-bis-2-nitrobenzoic acid ; ELISA ; enzyme-linked immunosorbent assay ; GAPDH ; glyceraldehyde-3-phosphate dehydrogenase ; Grx ; glutaredoxin ; HED ; 2-hydroxyethyl disulfide ; JAKs ; Janus protein tyrosine kinases ; JNK ; c-Jun N-terminal kinase ; MAPK ; mitogen-activated protein kinase ; MATII ; methionine adenosyltransferase II ; MM(PEG)24 ; Methyl-PEG24-Mal
- 刊名：Redox Biology
- 出版年：2015
- 出版时间：December 2015
- 年：2015
- 卷：6
- 期：Complete
- 页码：122-134
- 全文大小：2792 K
文摘
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Endogenous NO induces NADPH and reduces nucleotide biosynthesis in HepG2 cells.
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Trx1 and Grx1 have a pro-oxidant action on key proteins under nitrosative conditions.
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Trx1 and Grx1 hamper the antiproliferative action of NO in tumoral cells.
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Weakening of thiolic antioxidant defenses could help in the design of anti-tumoral therapies.