Emerging from NF-κB's shadow, SUMOylated IκBα represses transcription.
In this issue of Cancer Cell, Mulero and colleagues describe an NF-κB independent transcriptional repression function for SUMOylated IκBα. This compelling and provocative model links IκBα to the activity of the Polycomb repressors and provides a mechanism to link inflammatory signaling to skin homeostasis.
Institute for Cell and Molecular Biosciences, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne NE2 4HH, UK. neil.perkins@ncl.ac.uk
Neil D
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Perkins
D000818:Animals; D002843:Chromatin / Q000378:metabolism*; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism*; D000072000:NF-KappaB Inhibitor alpha; D012878:Skin Neoplasms / Q000378:metabolism*
D002843:Chromatin; D020672:I-kappa B Proteins; C000606204:NFKBIA protein, human; D000072000:NF-KappaB Inhibitor alpha