2009
DOI: 10.1371/journal.pone.0007036
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Exclusion of NFAT5 from Mitotic Chromatin Resets Its Nucleo-Cytoplasmic Distribution in Interphase

Abstract: BackgroundThe transcription factor NFAT5 is a major inducer of osmoprotective genes and is required to maintain the proliferative capacity of cells exposed to hypertonic stress. In response to hypertonicity, NFAT5 translocates to the nucleus, binds to regulatory regions of osmoprotective genes and activates their transcription. Besides stimulus-specific regulatory mechanisms, the activity of transcription factors in cycling cells is also regulated by the passage through mitosis, when most transcriptional proce… Show more

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Cited by 9 publications
(6 citation statements)
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“…2f–h ). In contrast to TEAD cytoplasmic localization, osmotic stress stimulates nuclear translocation of the transcription factor Nuclear Factor of Activated T-cells 5 (NFAT5) 15 , thus TEAD cytoplasmic translocation is a specific cellular response upon osmotic stress ( Supplementary Fig. 2i ).…”
Section: Main Textmentioning
confidence: 99%
“…2f–h ). In contrast to TEAD cytoplasmic localization, osmotic stress stimulates nuclear translocation of the transcription factor Nuclear Factor of Activated T-cells 5 (NFAT5) 15 , thus TEAD cytoplasmic translocation is a specific cellular response upon osmotic stress ( Supplementary Fig. 2i ).…”
Section: Main Textmentioning
confidence: 99%
“…BMDMs were cultured for 24 h on sterile glass coverslips coated with 0.01% w/v poly-L-lysine (Sigma-Aldrich). Cells were stimulated with 1 ng/ ml LPS for the indicated times and then fixed with 3% paraformaldehyde in 0.1 M phosphate buffer (pH 7.4), washed and permeabilized with wash buffer (0.5% NP-40 in PBS), and blocked with 10% FCS in wash buffer (33). Cells were then incubated with an Ab to p65/RelA (sc-372; Santa Cruz Biotechnology) in blocking solution, then with goat anti-rabbit IgG-FITC (F0382; Sigma-Aldrich).…”
Section: Immunocytochemistrymentioning
confidence: 99%
“…This domain acts as a dominant negative for NFAT5 as it competes for DNA binding and also displaces the endogenous dimers of NFAT5 ( 30 ). This DBD also gets progressively accumulated in a DNA-bound pool after successive rounds of cell division and thus may block access of endogenous NFAT5 to chromatin in a durable manner ( 78 ). NFAT5 DBD-transgenic mice had normal CD4 cellularity but fewer CD8 T cells in spleen and lymph nodes than non-transgenic controls.…”
Section: Osmostress-independent Regulation Of T Lymphocytes By Nfat5mentioning
confidence: 99%