Home
Deutsch
Advanced Search
Browse by ...
Publication overview
Contact persons
Help
DOI
 |
|
Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
Loss of intestinal crypt progenitor cells owing to inactivation of both Notch1 and Notch2 is accompanied by derepression of CDK inhibitors p27Kip1 and p57Kip2.
EMBO Rep. 9, 377-383 (2008)
The crucial role of individual Notch receptors and the mechanism by which they maintain intestinal crypt progenitor cells were assessed by using a series of inducible gut-specific Notch mutant mice. We found that Notch1 and Notch2 receptors function redundantly in the gut, as only simultaneous loss of both receptors results in complete conversion of proliferating crypt progenitors into post-mitotic goblet cells. This conversion correlates with the loss of Hes1 expression and derepression of the cyclin-dependent kinase (CDK) inhibitors p27Kip1 and p57Kip2. We also found that the promoter of both CDK inhibitor genes is occupied by the Notch effector Hes1 in wild-type crypt progenitor cells. Thus, our results indicate that Notch-mediated Hes1 expression contributes to the maintenance of the proliferative crypt compartment of the small intestine by transcriptionally repressing two CDK inhibitors.
Altmetric
Additional Metrics?
Edit extra informations
Login
Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Notch; intestine; CDKI; growth arrest; differentiation
ISSN (print) / ISBN
1469-221X
e-ISSN
1469-3178
Journal
EMBO Reports
Quellenangaben
Volume: 9,
Issue: 4,
Pages: 377-383
Publisher
EMBO Press
Reviewing status
Peer reviewed
Institute(s)
Research Unit Gene Vector (AGV)