PMID:16618808

Citation	Nguyen, BC, Lefort, K, Mandinova, A, Antonini, D, Devgan, V, Della Gatta, G, Koster, MI, Zhang, Z, Wang, J, Tommasi di Vignano, A, Kitajewski, J, Chiorino, G, Roop, DR, Missero, C and Dotto, GP (2006) Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation. Genes Dev. 20:1028-42
Abstract	Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation.
Links	PubMed PMC1472299 Online version:10.1101/gad.1406006
Keywords	Animals; Base Sequence; Cell Differentiation/physiology; DNA Primers; DNA-Binding Proteins/physiology; Humans; Keratinocytes/cytology; Mice; Promoter Regions, Genetic; RNA, Small Interfering; Receptor, Notch1/physiology; Trans-Activators/physiology; Transcription Factors; Tumor Suppressor Proteins/physiology
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.