ArticleFree radical biology & medicine2011
Activation of the glutaredoxin-1 gene by nuclear factor κB enhances signaling.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
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- Manganese Porphyrin Reduces Oxidative Stress in Vulnerable Parkin-NullAntioxidants (Basel, Switzerland) · 2025Article
- Redox homeostasis and inflammation in fibroblasts of patients with Friedreich Ataxia: a possible cross talk.Frontiers in molecular neuroscience · 2025Article
- The subcutaneous adipose transcriptome identifies a molecular signature of insulin resistance shared with visceral adipose.Obesity (Silver Spring, Md.) · 2024Article
- Glutaredoxin-1 modulates the NF-κB signaling pathway to activate inducible nitric oxide synthase in experimental necrotizing enterocolitis.Molecular therapy. Methods & clinical development · 2024Article
- Glutaredoxin: Discovery, redox defense and much more.Redox biology · 2021Review
- Characterization of cellular oxidative stress response by stoichiometric redox proteomics.American journal of physiology. Cell physiology · 2021Review
- Redox Regulation, Oxidative Stress, and Inflammation in Group 3 Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Review
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- Glycolytic overload-driven dysfunction of periodontal ligament fibroblasts in high glucose concentration, corrected by glyoxalase 1 inducer.BMJ open diabetes research & care · 2020Article
- Endoplasmic reticulum stress and glutathione therapeutics in chronic lung diseases.Redox biology · 2020Review
- Redox RegulationAntioxidants & redox signaling · 2020Review
- Dysregulation of the glutaredoxin/American journal of physiology. Cell physiology · 2020Article
- The Role of Meat Protein in Generation of Oxidative Stress and Pathophysiology of Metabolic Syndromes.Food science of animal resources · 2020Review
- Production of adeno-associated virus vectors for in vitro and in vivo applications.Scientific reports · 2019Article
- Erythrocyte and plasma oxidative stress appears to be compensated in patients with sickle cell disease during a period of relative health, despite the presence of known oxidative agents.Free radical biology & medicine · 2019Article
- Critical Roles of Glutaredoxin in Brain Cells-Implications for Parkinson's Disease.Antioxidants & redox signaling · 2019Review
- Article
- Glutaredoxin-1 Deficiency Causes Fatty Liver and Dyslipidemia by Inhibiting Sirtuin-1.Antioxidants & redox signaling · 2017Article
- Redox regulation of ischemic limb neovascularization - What we have learned from animal studies.Redox biology · 2017Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcription factor nuclear factor κB (NF-κB) is a critical regulator of inflammation and immunity and is negatively regulated via S-glutathionylation. The inhibitory effect of S-glutathionylation is overcome by glutaredoxin-1 (Grx1), which under physiological conditions catalyzes deglutathionylation and enhances NF-κB activation. The mechanisms whereby expression of the Glrx1 gene is regulated remain unknown. Here we examined the role of NF-κB in regulating activation of Glrx1. Transgenic mice that express a doxycycline-inducible constitutively active version of inhibitory κB kinase-β (CA-IKKβ) demonstrate elevated expression of Grx1. Transient transfection of CA-IKKβ also resulted in significant induction of Grx1. A 2-kb region of the Glrx1 promoter that contains two putative NF-κB binding sites was activated by CA-IKKβ, RelA/p50, and lipopolysaccharide (LPS). Chromatin immunoprecipitation experiments confirmed binding of RelA to the promoter of Glrx1 in response to LPS. Stimulation of C10 lung epithelial cells with LPS caused transient increases in Grx1 mRNA expression and time-dependent increases in S-glutathionylation of IKKβ. Overexpression of Grx1 decreased S-glutathionylation of IKKβ, prolonged NF-κB activation, and increased levels of proinflammatory mediators. Collectively, this study demonstrates that the Glrx1 gene is positively regulated by NF-κB and suggests a feed-forward mechanism to promote NF-κB signaling by decreasing S-glutathionylation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.