ArticleEndocrinology2009
S-glutathionylation impairs signal transducer and activator of transcription 3 activation and signaling.
Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 124 citations in OpenAlex.
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- Reactive Sulfur Species and Protein Persulfidation: An Emerging Redox Axis in Human Health and Disease.Current issues in molecular biology · 2025Review
- Oxidative stress-induced CDO1 glutathionylation regulates cysteine metabolism and sustains redox homeostasis under ionizing radiation.Redox biology · 2025Article
- Navigating the redox landscape: reactive oxygen species in regulation of cell cycle.Redox report : communications in free radical research · 2024Review
- Disulfide stress and its role in cardiovascular diseases.Redox biology · 2024Review
- Glutathione dynamics in subcellular compartments and implications for drug development.Current opinion in chemical biology · 2024Review
- Robust AMBER Force Field Parameters for Glutathionylated Cysteines.International journal of molecular sciences · 2023Article
- The mitochondrial succinate dehydrogenase complex controls the STAT3-IL-10 pathway in inflammatory macrophages.iScience · 2023Article
- STAT proteins in cancer: orchestration of metabolism.Nature reviews. Cancer · 2023Review
- Cystathionine β-synthase overexpression drives metastatic dissemination in pancreatic ductal adenocarcinoma via inducing epithelial-to-mesenchymal transformation of cancer cells.Redox biology · 2022Article
- Bilateral Superior Cervical Sympathectomy Activates Signal Transducer and Activator of Transcription 3 Signal to Alleviate Myocardial Ischemia-Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Article
- STAT proteins: a kaleidoscope of canonical and non-canonical functions in immunity and cancer.Journal of hematology & oncology · 2021Review
- Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function.Basic research in cardiology · 2021Review
- The antioxidant role of STAT3 in methylmercury-induced toxicity in mouse hypothalamic neuronal GT1-7 cell line.Free radical biology & medicine · 2021Article
- Redox regulation of immunity and the role of small molecular weight thiols.Redox biology · 2021Article
- Hemistepsin a Induces Apoptosis of Hepatocellular Carcinoma Cells by Downregulating STAT3.International journal of molecular sciences · 2021Article
- Glutathione S-Transferases in Cancer.Antioxidants (Basel, Switzerland) · 2021Review
- S-glutathionylation, friend or foe in cardiovascular health and disease.Redox biology · 2020Review
- Perspectives Regarding the Intersections between STAT3 and Oxidative Metabolism in Cancer.Cells · 2020Review
- Redox Regulation of STAT1 and STAT3 Signaling.International journal of molecular sciences · 2020Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
S-glutathionylation is a physiological, reversible protein modification of cysteine residues with glutathione in response to mild oxidative stress. Because the key cell growth regulator signal transducer and activator of transcription (STAT) 3 is particularly susceptible to redox regulation, we hypothesized that oxidative modification of cysteine residues of STAT3 by S-glutathionylation may occur. Herein, we show that the cysteine residues of STAT3 are modified by a thiol-alkylating agent and are the targets of S-glutathionylation. STAT3 protein thiol reactivity was reversibly attenuated with concomitant increase in the S-glutathionylation of STAT3 upon treatment of human HepG2 hepatoma cells with pyrrolidine dithiocarbamate, glutathione disulfide, or diamide. Under these conditions there was a marked reduction in IL-6-dependent STAT3 signaling, including decreased STAT3 tyrosine phosphorylation, loss in nuclear accumulation of STAT3, and impaired expression of target genes, such as fibrinogen-gamma. In a cell-free system, diamide induced glutathionylation of STAT3, which was decreased upon addition of glutaredoxin (GRX)-1, a deglutathionylation enzyme, or the reducing agent, dithiothreitol. Glutathionylated STAT3 was a poor Janus protein tyrosine kinase 2 substrate in vitro, and it exhibited low DNA-binding activity. Cellular GRX-1 activity was inhibited by diamide and pyrrolidine dithiocarbamate treatment; however, ectopic expression of GRX-1 was accompanied by a modest increase in phosphorylation, nuclear translocation, and DNA-binding ability of STAT3 in response to IL-6. These results are the first to show S-glutathionylation of STAT3, a modification that may exert regulatory function in STAT3 signaling.
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What OpenQuestion holds
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.