Molecular Biology of the Cell Call for Nominations: MBC Editor-in-Chief

Home Help [Feedback] [For Subscribers] [Archive] [Search] --
QUICK SEARCH:   [advanced]


     

MBC in Press, published online ahead of print March 29, 2006
Mol. Biol. Cell 10.1091/mbc.E06-01-0052

A more recent version of this article appeared on June 1, 2006
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
E06-01-0052v1
17/6/2572    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bachar-Dahan, L.
Right arrow Articles by Gazit, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bachar-Dahan, L.
Right arrow Articles by Gazit, A.

Submitted on January 18, 2006
Revised on February 27, 2006
Accepted on March 16, 2006

Engrailed-1 Negatively Regulates {beta}-Catenin Transcriptional Activity by Destabilizing {beta}-Catenin via a GSK-3{beta}-independent Pathway

Liora Bachar-Dahan, Janna Goltzmann, Abraham Yaniv, and Arnona Gazit

Department of Human Microbiology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel

Monitoring Editor: Carl-Henrik Heldin

The Wnt signaling pathway plays a major role in development and upon deregulation it is implicated in neoplasia. The hallmark of the canonical Wnt signal is the protection of {beta}-catenin from ubiquitination and proteasomal degradation induced by GSK-3{beta} inhibition. The stabilized {beta}-catenin translocates to the nucleus where it binds to TCF/LEF transcription factors, activating the expression of Wnt target genes. In the absence of Wnt signal, TCF/LEF bind to Groucho (Gro)/TLE corepressors and repress Wnt target genes. Gro/TLE bind also to Engrailed (En) transcription factors mediating En repressive activity on En target genes. Here we present data suggesting that En-1 serves also as a negative regulator of {beta}-catenin trancriptional activity; however, its repressive effect is independent of Gro/TLE. Our data suggest that En-1 acts by destabilizing {beta}-catenin via a proteasomal degradation pathway that is GSK-3{beta}- independent. Moreover, since En-1-mediated {beta}-catenin degradation is also Siah-independent, our data imply that En-1 exerts its repressive effect by a novel mechanism negatively controling the level of {beta}-catenin.

Address correspondence to: Arnona Gazit (micro1{at}post.tau.ac.il)




This article has been cited by other articles:


Home page
 Mol Hum ReprodHome page
B. Novakovic, V. Rakyan, H.K. Ng, U. Manuelpillai, C. Dewi, N.C. Wong, R. Morley, T. Down, S. Beck, J.M. Craig, et al.
Specific tumour-associated methylation in normal human term placenta and first-trimester cytotrophoblasts
Mol. Hum. Reprod., September 1, 2008; 14(9): 547 - 554.
[Abstract] [Full Text] [PDF]

Home page
 Mol Cancer ResHome page
P. Karpinski, D. Ramsey, Z. Grzebieniak, M. M. Sasiadek, and N. Blin
The CpG Island Methylator Phenotype Correlates with Long-Range Epigenetic Silencing in Colorectal Cancer
Mol. Cancer Res., April 1, 2008; 6(4): 585 - 591.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Copyright © 2006 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.