Journal
GENES & DEVELOPMENT
Volume 20, Issue 8, Pages 1028-1042Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1406006
Keywords
keratinocyte; stem cells; Notch; p63; interferon -responsive genes; HES/HERP family members
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Funding
- NCI NIH HHS [R01 CA073796, CA16038, P01 CA016038, CA73796] Funding Source: Medline
- NIAMS NIH HHS [AR39190, R01 AR039190] Funding Source: Medline
- Telethon [TGM06S01, TGM03P14] Funding Source: Medline
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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 Notch 1-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.
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