Published online 12 July 2005
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NFAT5 binds to the TNF promoter distinctly from NFATp, c, 3 and 4, and activates TNF transcription during hypertonic stress alone
CBR Institute for Biomedical Research, Department of Pathology, Harvard Medical School 800 Huntington Avenue, Boston, MA 02115, USA
*To whom correspondence should be addressed. Tel: +1 617 278 3351; Fax: +1 617 278 3454; Email: goldfeld{at}cbrinstitute.org
Received April 1, 2005. Revised June 23, 2005. Accepted June 23, 2005.
Tumor necrosis factor (TNF) is a pro-inflammatory cytokine that plays an important role in a variety of infectious and autoimmune disorders. Its transcription is regulated in a stimulus- and cell-type-specific manner via the recruitment of distinct DNA/activator complexes forming secondary structures or enhanceosomes. NFATp, a member of the nuclear factor of activated T cells (NFAT) family of transcription factors, plays a critical role in TNF gene regulation under a variety of conditions. In this study, we show that NFAT5, the most recently described NFAT family member, binds to the TNF promoter in a manner distinct from other NFAT proteins and is a key mediator in the activation of TNF gene transcription during hypertonic stress alone.
Present address: Cristina Lopez-Rodriguez, Immunopathology unit, Department of Health and Experimental Sciences, University Pompeu Fabra, c/o Dr Aiguader 80, 08003 Barcelona, Spain
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors
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