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本文引用的文献

1
Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition.耐药物持久性癌细胞易受谷胱甘肽过氧化物酶4(GPX4)抑制的影响。
Nature. 2017 Nov 9;551(7679):247-250. doi: 10.1038/nature24297. Epub 2017 Nov 1.
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Chemical Proteomics Identifies Druggable Vulnerabilities in a Genetically Defined Cancer.化学蛋白质组学鉴定出基因定义癌症中的可药物化靶点。
Cell. 2017 Oct 19;171(3):696-709.e23. doi: 10.1016/j.cell.2017.08.051. Epub 2017 Sep 28.
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Dependency of a therapy-resistant state of cancer cells on a lipid peroxidase pathway.癌细胞的治疗抗性状态对脂质过氧化酶途径的依赖性。
Nature. 2017 Jul 27;547(7664):453-457. doi: 10.1038/nature23007. Epub 2017 Jul 5.
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Reactive oxygen species are required for driving efficient and sustained aerobic glycolysis during CD4+ T cell activation.在CD4+ T细胞活化过程中,活性氧对于驱动高效且持续的有氧糖酵解是必需的。
PLoS One. 2017 Apr 20;12(4):e0175549. doi: 10.1371/journal.pone.0175549. eCollection 2017.
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Glutathione Primes T Cell Metabolism for Inflammation.谷胱甘肽激活 T 细胞代谢以缓解炎症。
Immunity. 2017 Apr 18;46(4):675-689. doi: 10.1016/j.immuni.2017.03.019.
6
Systemic depletion of L-cyst(e)ine with cyst(e)inase increases reactive oxygen species and suppresses tumor growth.用胱硫醚酶对L-胱氨酸进行全身消耗会增加活性氧并抑制肿瘤生长。
Nat Med. 2017 Jan;23(1):120-127. doi: 10.1038/nm.4232. Epub 2016 Nov 21.
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Suppressors of Superoxide-HO Production at Site I of Mitochondrial Complex I Protect against Stem Cell Hyperplasia and Ischemia-Reperfusion Injury.线粒体复合物I位点I处超氧化物-HO产生的抑制剂可预防干细胞增生和缺血再灌注损伤。
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Cancer Res. 2016 Aug 1;76(15):4430-42. doi: 10.1158/0008-5472.CAN-16-0530. Epub 2016 Jun 8.
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Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling.线粒体产生超氧化物和过氧化氢作为线粒体氧化还原信号的来源。
Free Radic Biol Med. 2016 Nov;100:14-31. doi: 10.1016/j.freeradbiomed.2016.04.001. Epub 2016 Apr 13.
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Reductive carboxylation supports redox homeostasis during anchorage-independent growth.还原性羧化作用在非锚定依赖性生长过程中维持氧化还原稳态。
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癌症和 T 细胞中氧化还原平衡的调节。

Regulation of redox balance in cancer and T cells.

机构信息

From the Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.

From the Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611

出版信息

J Biol Chem. 2018 May 18;293(20):7499-7507. doi: 10.1074/jbc.TM117.000257. Epub 2017 Dec 27.

DOI:10.1074/jbc.TM117.000257
PMID:29282291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5961053/
Abstract

Reactive oxygen species (ROS) mediate redox signaling necessary for numerous cellular functions. Yet, high levels of ROS in cells and tissues can cause damage and cell death. Therefore, regulation of redox homeostasis is essential for ROS-dependent signaling that does not incur cellular damage. Cells achieve this optimal balance by coordinating ROS production and elimination. In this Minireview, we discuss the mechanisms by which proliferating cancer and T cells maintain a carefully controlled redox balance. Greater insight into such redox biology may enable precisely targeted manipulation of ROS for effective medical therapies against cancer or immunological disorders.

摘要

活性氧 (ROS) 介导的氧化还原信号对于许多细胞功能是必需的。然而,细胞和组织中高水平的 ROS 会导致损伤和细胞死亡。因此,对于不引起细胞损伤的 ROS 依赖性信号,氧化还原稳态的调节是必不可少的。细胞通过协调 ROS 的产生和消除来实现这种最佳平衡。在这篇简评中,我们讨论了增殖的癌症和 T 细胞维持精细控制的氧化还原平衡的机制。对这种氧化还原生物学的更深入了解可能使我们能够精确地操纵 ROS,从而为癌症或免疫性疾病的有效医学治疗提供靶向治疗。