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López-Rodríguez, C. et al.

Loss of NFAT5 results in renal atrophy and lack of tonicity-responsive gene expression.

The transcription factor NFAT5/TonEBP, a member of the NFAT/Rel family of transcription factors, has been implicated in diverse cellular responses, including the response to osmotic stress, integrin-dependent cell migration, T cell activation, and the Ras pathway in Drosophila. To clarify the in vivo role of NFAT5, we generated NFAT5-null mice. Homozygous mutants were genetically underrepresented after embryonic day 14. 5. Surviving mice manifested a progressive and profound atrophy of the kidney medulla with impaired activation of several osmoprotective genes, including those encoding aldose reductase, Na+/Cl--coupled betaine/gamma-aminobutyric acid transporter, and the Na+/myo-inositol cotransporter. The aldose reductase gene is controlled by a tonicity-responsive enhancer, which was refractory to hypertonic stress in fibroblasts lacking NFAT5, establishing this enhancer as a direct transcriptional target of NFAT5. Our findings demonstrate a central role for NFAT5 as a tonicity-responsive transcription factor required for kidney homeostasis and function.[1]

References

Loss of NFAT5 results in renal atrophy and lack of tonicity-responsive gene expression. López-Rodríguez, C., Antos, C.L., Shelton, J.M., Richardson, J.A., Lin, F., Novobrantseva, T.I., Bronson, R.T., Igarashi, P., Rao, A., Olson, E.N. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]

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