ArticleProceedings of the National Academy of Sciences of the United States of America1999
Tonicity-responsive enhancer binding protein, a rel-like protein that stimulates transcription in response to hypertonicity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 262 papers.
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Who cites it
262 citing papers in PubMed, 582 citations in OpenAlex.
- Tonicity drives collecting duct maturation in the mammalian kidney.Nature communications · 2026Article
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Identification of Sodium/Myo-Inositol Transporter 1 as a Major Determinant of Arterial Contractility.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Nuclear factor of activated T cells as a driver of tumor progression and a target for precision therapy.Animal models and experimental medicine · 2026Review
- TonEBP as a key regulator of hypothalamic leptin signaling and resistance.Cellular and molecular life sciences : CMLS · 2026Article
- Hepatocyte TonEBP promotes metabolic stress-induced hepatic fibroinflammation involving transcriptional activation of ELR⁺ CXC chemokines.Cell death discovery · 2026Article
- NFAT5 dictates crosstalk between intestinal epithelial regenerative capacity and microbiota in murine colitis models.The Journal of clinical investigation · 2025Article
- Dmrt2 and Hmx2 direct intercalated cell diversity in the mammalian kidney through antagonistic and supporting regulatory processes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Neuronal CCL2 responds to hyperglycaemia and contributes to anxiety disorders in the context of diabetes.Nature metabolism · 2025Article
- NF-κB-mediated EAAT3 upregulation in antioxidant defense and ferroptosis sensitivity in lung cancer.Cell death & disease · 2025Article
- Direct ionic stress sensing and mitigation by the transcription factor NFAT5.Science advances · 2025Article
- High salt-induced osmotic stress differentially modulates hepatocellular and renal carcinoma cell proliferation.Frontiers in oncology · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Hyperosmolar stress induces monocyte chemoattractant protein 1 expression in retinal pigmented epithelial arising retinal pigmented epithelial 19 cells.Molecular vision · 2025Article
- Adequate post-ischemic reperfusion of the mouse brain requires endothelial NFAT5.Acta neuropathologica communications · 2024Article
- NFAT5 governs cellular plasticity-driven resistance to KRAS-targeted therapy in pancreatic cancer.The Journal of experimental medicine · 2024Article
- HES1 potentiates high salt stress response as an enhancer of NFAT5-DNA binding.Communications biology · 2024Article
- Sodium chloride in the tumor microenvironment enhances T cell metabolic fitness and cytotoxicity.Nature immunology · 2024Article
- Article
- TonEBP inhibits ciliogenesis by controlling aurora kinase A and regulating centriolar satellite integrity.Cell communication and signaling : CCS · 2024Article
202 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Hypertonicity (most often present as high salinity) is stressful to the cells of virtually all organisms. Cells survive in a hypertonic environment by increasing the transcription of genes whose products catalyze cellular accumulation of compatible osmolytes. In mammals, the kidney medulla is normally hypertonic because of the urinary concentrating mechanism. Cellular accumulation of compatible osmolytes in the renal medulla is catalyzed by the sodium/myo-inositol cotransporter (SMIT), the sodium/chloride/betaine cotransporter, and aldose reductase (synthesis of sorbitol). The importance of compatible osmolytes is underscored by the necrotic injury of the renal medulla and subsequent renal failure that results from the inhibition of SMIT in vivo by administration of a specific inhibitor. Tonicity-responsive enhancers (TonE) play a key role in hypertonicity-induced transcriptional stimulation of SMIT, sodium/chloride/betaine cotransporter, and aldose reductase. We report the cDNA cloning of human TonE binding protein (TonEBP), a transcription factor that stimulates transcription through its binding to TonE sequences via a Rel-like DNA binding domain. Western blot and immunohistochemical analyses of cells cultured in hypertonic medium reveal that exposure to hypertonicity elicits slow activation of TonEBP, which is the result of an increase in TonEBP amount and translocation to the nucleus.
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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.