ArticleScience signaling2009
Brx mediates the response of lymphocytes to osmotic stress through the activation of NFAT5.
Article in Science signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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The trial behind it
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Who cites it
59 citing papers in PubMed, 94 citations in OpenAlex.
- Salt and chronic kidney disease.Nature reviews. Nephrology · 2026Review
- Direct ionic stress sensing and mitigation by the transcription factor NFAT5.Science advances · 2025Article
- The SIRT5-JIP4 interaction promotes osteoclastogenesis by modulating RANKL-induced signaling transduction.Cell communication and signaling : CCS · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Article
- Direct ionic stress sensing and mitigation by the transcription factor NFAT5.bioRxiv : the preprint server for biology · 2023Article
- High Salt Promotes Inflammatory and Fibrotic Response in Peritoneal Cells.International journal of molecular sciences · 2023Article
- Serine protease 35 regulates the fibroblast matrisome in response to hyperosmotic stress.Science advances · 2023Article
- Their last will and testament: dying immune cells protect the urinary system with extracellular DNA traps.Kidney international · 2023Article
- The modulatory effect of high salt on immune cells and related diseases.Cell proliferation · 2022Review
- Innate Bacteriostatic Mechanisms Defend the Urinary Tract.Annual review of physiology · 2022Review
- NFAT5-Mediated Signalling Pathways in Viral Infection and Cardiovascular Dysfunction.International journal of molecular sciences · 2021Review
- Review
- TonEBP regulates the hyperosmotic expression of aquaporin 1 and 5 in the intervertebral disc.Scientific reports · 2021Article
- Computational System Level Approaches for Discerning Reciprocal Regulation of IL10 and IL12 in Leishmaniasis.Frontiers in genetics · 2021Article
- Obesity ‑ a risk factor for increased COVID‑19 prevalence, severity and lethality (Review).Molecular medicine reports · 2020Review
- High-salt diet inhibits tumour growth in mice via regulating myeloid-derived suppressor cell differentiation.Nature communications · 2020Article
- A Membranome-Centered Approach Defines Novel Biomarkers for Cellular Subtypes in the Intervertebral Disc.Cartilage · 2020Article
- Sodium homeostasis in the tumour microenvironment.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- A-Kinase Anchoring Protein 13 (AKAP13) Augments Progesterone Signaling in Uterine Fibroid Cells.The Journal of clinical endocrinology and metabolism · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Extracellular hyperosmolarity, or osmotic stress, generally caused by differences in salt and macromolecule concentrations across the plasma membrane, occurs in lymphoid organs and at inflammatory sites. The response of immune cells to osmotic stress is regulated by nuclear factor of activated T cells 5 (NFAT5), a transcription factor that induces the expression of hyperosmolarity-responsive genes and stimulates cytokine production. We report that the guanine nucleotide exchange factor (GEF) Brx [also known as protein kinase A-anchoring protein 13 (AKAP13)] is essential for the expression of nfat5 in response to osmotic stress, thus transmitting the extracellular hyperosmolarity signal and enabling differentiation of splenic B cells and production of immunoglobulin. This process required the activity of p38 mitogen-activated protein kinase (MAPK) and NFAT5 and involved a physical interaction between Brx and c-Jun N-terminal kinase (JNK)-interacting protein 4 (JIP4), a scaffold molecule specific to activation of the p38 MAPK cascade. Our results indicate that Brx integrates the responses of immune cells to osmotic stress and inflammation by elevating intracellular osmolarity and stimulating the production of cytokines.
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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.