JBC Advanced Glycation Endproducts

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on September 10, 2004
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
279/37/38313    most recent
M401610200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Pinte, S.
Right arrow Articles by Leprince, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pinte, S.
Right arrow Articles by Leprince, D.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Papers In Press, published online ahead of print July 1, 2004
J. Biol. Chem, 10.1074/jbc.M401610200
Submitted on February 13, 2004
Revised on July 1, 2004
Accepted on July 1, 2004

The tumor suppressor gene HIC1 (hypermethylated in cancer 1) is a sequence-specific transcriptional repressor : Definition of its consensus binding sequence and analysis of its DNA-binding and repressive properties

Sébastien Pinte, Nicolas Stankovic-Valentin, Sophie Deltour, Brian R. Rood, Cateline Guerardel, and Dominique Leprince

CNRS UMR 8526, Institut de Biologie de LILLE-Institut Pasteur de Lille, Lille 59021

Corresponding Author: dominique.leprince{at}ibl.fr

HIC1 (Hypermethylated in Cancer 1) is a tumor suppressor gene located at chromosome 17p13.3, a region frequently hypermethylated or deleted in human tumors and in a contiguous-gene syndrome, the Miller-Dieker syndrome’s. HIC1 is a transcriptional repressor containing five Krüppel-like C2H2 zinc fingers and an N-terminal dimerization and autonomous repression domain called BTB/POZ. Whereas some of the HIC1 transcriptional repression mechanisms have been recently deciphered, target genes are still to be discovered. In this study, we determined the consensus binding sequence for HIC1 and investigated its DNA-binding properties. Using a selection and amplification of binding sites (SAAB) technique, we identified the sequence 5’-C/GNGC/GGGGCAC/ACC-3’ as an optimal binding site. In silico and functional analyses fully validated this consensus and highlighted a GGCA core motif bound by zinc fingers 3 and 4. The BTB/POZ domain inhibits the binding of HIC1 to a single site but mediates cooperative binding to a probe containing five concatemerized binding sites, a property shared by other BTB/POZ proteins. Finally, full-length HIC1 proteins transiently expressed in RK13 cells and more importantly, endogenous HIC1 proteins from the DAOY medulloblastoma cell line, repress the transcription of a reporter gene through their direct binding to these sites, as confirmed by ChIP experiments. The definition of the HIC1 specific DNA-binding sequence as well as the requirement for multiple sites for optimal binding of the full-length protein are mandatory prerequisites for the identification and analyses of bona fide HIC1 target genes.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 Genes Dev.Home page
K. J. Briggs, I. M. Corcoran-Schwartz, W. Zhang, T. Harcke, W. L. Devereux, S. B. Baylin, C. G. Eberhart, and D. N. Watkins
Cooperation between the Hic1 and Ptch1 tumor suppressors in medulloblastoma
Genes & Dev., March 15, 2008; 22(6): 770 - 785.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
N. Stankovic-Valentin, S. Deltour, J. Seeler, S. Pinte, G. Vergoten, C. Guerardel, A. Dejean, and D. Leprince
An Acetylation/Deacetylation-SUMOylation Switch through a Phylogenetically Conserved {psi}KXEP Motif in the Tumor Suppressor HIC1 Regulates Transcriptional Repression Activity
Mol. Cell. Biol., April 1, 2007; 27(7): 2661 - 2675.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
C. Hellerbrand, E. Bumes, F. Bataille, W. Dietmaier, R. Massoumi, and A. K. Bosserhoff
Reduced expression of CYLD in human colon and hepatocellular carcinomas
Carcinogenesis, January 1, 2007; 28(1): 21 - 27.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
D. Arlt, W. Huber, U. Liebel, C. Schmidt, M. Majety, M. Sauermann, H. Rosenfelder, S. Bechtel, A. Mehrle, D. Bannasch, et al.
Functional Profiling: From Microarrays via Cell-Based Assays to Novel Tumor Relevant Modulators of the Cell Cycle
Cancer Res., September 1, 2005; 65(17): 7733 - 7742.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
T. Morinaga, A. Enomoto, Y. Shimono, F. Hirose, N. Fukuda, A. Dambara, M. Jijiwa, K. Kawai, K. Hashimoto, M. Ichihara, et al.
GDNF-inducible zinc finger protein 1 is a sequence-specific transcriptional repressor that binds to the HOXA10 gene regulatory region
Nucleic Acids Res., July 26, 2005; 33(13): 4191 - 4201.
[Abstract] [Full Text] [PDF]

Home page
 J. Cell Sci.Home page
K. F. Kelly, A. A. Otchere, M. Graham, and J. M. Daniel
Nuclear import of the BTB/POZ transcriptional regulator Kaiso
J. Cell Sci., December 1, 2004; 117(25): 6143 - 6152.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2004 by the American Society for Biochemistry and Molecular Biology.