Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69. (Q42526186)

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English	Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69.	scientific article

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12244325

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1 November 2017

title

Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69. (English)

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Europe PubMed Central

PubMed publication ID

12244325

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1 November 2017

main subject

apoptotic process

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author

Judith Haendeler

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1

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Europe PubMed Central

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12244325

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1 November 2017

Bradford C. Berk

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4

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Europe PubMed Central

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12244325

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1 November 2017

Stefanie Dimmeler

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12244325

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1 November 2017

Andreas Zeiher

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5

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Andreas M Zeiher

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Europe PubMed Central

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12244325

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1 November 2017

Verena Tischler

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3

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Verena Tischler

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12244325

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1 November 2017

author name string

Jörg Hoffmann

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2

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12244325

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1 November 2017

publication date

1 October 2002

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12244325

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1 November 2017

published in

Nature Cell Biology

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12244325

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1 November 2017

volume

4

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12244325

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1 November 2017

issue

10

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12244325

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1 November 2017

page(s)

743-749

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12244325

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cites work

Reactive oxygen species, antioxidants, and the mammalian thioredoxin system

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Early embryonic lethality caused by targeted disruption of the mouse thioredoxin gene.

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From RNA to DNA, why so many ribonucleotide reductases?

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Redox regulation by thioredoxin superfamily; protection against oxidative stress and aging

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AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1

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Thioredoxin regulates the DNA binding activity of NF-kappa B by reduction of a disulphide bond involving cysteine 62

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https://api.crossref.org/works/10.1038%2FNCB851

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Distinct effects of thioredoxin and antioxidants on the activation of transcription factors NF-kappa B and AP-1.

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Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.

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The L-arginine-nitric oxide pathway

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Role of endothelial nitric oxide synthase in endothelial cell migration

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Nitric oxide-an endothelial cell survival factor.

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S-nitrosylation of proteins with nitric oxide: synthesis and characterization of biologically active compounds

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NO: an inhibitor of cell death

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7 January 2021

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S-nitrosylation regulates apoptosis.

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An apoptotic model for nitrosative stress

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TNFalpha and oxLDL reduce protein S-nitrosylation in endothelial cells

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Nitrosylation. the prototypic redox-based signaling mechanism.

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Fas-induced caspase denitrosylation

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(S)NO signals: translocation, regulation, and a consensus motif

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Oxidative modifications in nitrosative stress

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Protein S-nitrosylation: a physiological signal for neuronal nitric oxide

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Regulation of gene expression by reactive oxygen

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Redox regulation of cellular activation

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The roles of thioredoxin in protection against oxidative stress-induced apoptosis in SH-SY5Y cells

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Thiol reducing agents modulate induced apoptosis in porcine endothelial cells

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Reactive oxygen species and vascular cell apoptosis in response to angiotensin II and pro-atherosclerotic factors

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7 January 2021

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Triggering and modulation of apoptosis by oxidative stress

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7 January 2021

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Molecular characterization and localization of the NAD(P)H oxidase components gp91-phox and p22-phox in endothelial cells

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7 January 2021

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Nitric oxide reversibly inhibits seven members of the caspase family via S-nitrosylation

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7 January 2021

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Suppression of apoptosis by nitric oxide via inhibition of interleukin-1beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases

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https://api.crossref.org/works/10.1038%2FNCB851

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7 January 2021

based on heuristic

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Effects of redox-related congeners of NO on apoptosis and caspase-3 activity

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Suppression of neuronal apoptosis by S-nitrosylation of caspases

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The skeletal muscle calcium release channel: coupled O2 sensor and NO signaling functions

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Export by red blood cells of nitric oxide bioactivity

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Cysteine-3635 is responsible for skeletal muscle ryanodine receptor modulation by NO

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The third cytoplasmic loop of the angiotensin II type 1 receptor exerts differential effects on extracellular signal-regulated kinase (ERK1/ERK2) and apoptosis via Ras- and Rap1-dependent pathways

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based on heuristic

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Oxidized low-density lipoprotein induces apoptosis of human endothelial cells by activation of CPP32-like proteases. A mechanistic clue to the 'response to injury' hypothesis.

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c-Jun N-terminal kinase (JNK) repression during the inflammatory response? Just say NO.

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https://api.crossref.org/works/10.1038%2FNCB851

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7 January 2021

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Identifiers

DOI

10.1038/NCB851

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Europe PubMed Central

PubMed publication ID

12244325

retrieved

1 November 2017

PubMed publication ID

12244325

1 reference

stated in

Europe PubMed Central

PubMed publication ID

12244325

retrieved

1 November 2017

 

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