Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation

Details

Serval ID
serval:BIB_C0921040B4B8
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation
Journal
Genes and Development
Author(s)
Nguyen  B. C., Lefort  K., Mandinova  A., Antonini  D., Devgan  V., Della Gatta  G., Koster  M. I., Zhang  Z., Wang  J., Tommasi di Vignano  A., Kitajewski  J., Chiorino  G., Roop  D. R., Missero  C., Dotto  G. P.
ISSN
0890-9369 (Print)
Publication state
Published
Issued date
04/2006
Volume
20
Number
8
Pages
1028-42
Notes
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't --- Old month value: Apr 15
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.
Keywords
Animals Base Sequence Cell Differentiation/*physiology DNA Primers DNA-Binding Proteins/*physiology Humans Keratinocytes/*cytology Mice Promoter Regions (Genetics) RNA, Small Interfering Receptor, Notch1/*physiology Trans-Activators/*physiology Tumor Suppressor Proteins/*physiology
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 14:59
Last modification date
20/08/2019 15:35
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