ArticleScientific reports2022
The nuclear factor of activated T cells 5 (NFAT5) contributes to the renal corticomedullary differences in gene expression.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Dissecting hypertonicity- and NFAT5-dependent gene expression programs in mpkCCD cells.Physiological reports · 2026Article
- BPGM shapes NFAT5-driven cellular responses.Cellular and molecular life sciences : CMLS · 2026Article
- Regulation of renal aquaporins: implications in tubular epithelial integrity.Biochemical Society transactions · 2026Review
- Long Non-coding RNA MIR22HG Alleviates Ischemic Acute Kidney Injury by Targeting the miR-134-5p/NFAT5 axis.Inflammation · 2025Article
- Unlocking the therapeutic potential of the NFAT pathway in kidney diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Thick Ascending Limb Specific Inactivation of Myh9 and Myh10 Myosin Motors Results in Progressive Kidney Disease and Drives Sex-specific Cellular Adaptation in the Distal Nephron and Collecting Duct.Function (Oxford, England) · 2025Article
- Segment specific loss of NFAT5 function in the kidneys is sufficient to induce a global kidney injury like phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Role of LncRNA in Trauma Susceptibility and Resilience to Post-Traumatic Stress Disorder (PTSD): A Pilot Study in the African American Population.Neuropsychiatric disease and treatment · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Answering the Cell Stress Call: Satellite Non-Coding Transcription as a Response Mechanism.Biomolecules · 2024Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The corticomedullary osmotic gradient between renal cortex and medulla induces a specific spatial gene expression pattern. The factors that controls these differences are not fully addressed. Adaptation to hypertonic environment is mediated by the actions of the nuclear factor of activated T-cells 5 (NFAT5). NFAT5 induces the expression of genes that lead to intracellular accumulation of organic osmolytes. However, a systematical analysis of the NFAT5-dependent gene expression in the kidneys was missing. We used primary cultivated inner medullary collecting duct (IMCD) cells from control and NFAT5 deficient mice as well as renal cortex and inner medulla from principal cell specific NFAT5 deficient mice for gene expression profiling. In primary NFAT5 deficient IMCD cells, hyperosmolality induced changes in gene expression were abolished. The majority of the hyperosmolality induced transcripts in primary IMCD culture were determined to have the greatest expression in the inner medulla. Loss of NFAT5 altered the expression of more than 3000 genes in the renal cortex and more than 5000 genes in the inner medulla. Gene enrichment analysis indicated that loss of NFAT5 is associated with renal inflammation and increased expression of kidney injury marker genes, like lipocalin-2 or kidney injury molecule-1. In conclusion we show that NFAT5 is a master regulator of gene expression in the kidney collecting duct and in vivo loss of NFAT function induces a kidney injury like phenotype.
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