JBC

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Originally published In Press as doi:10.1074/jbc.C100095200 on April 10, 2001

J. Biol. Chem., Vol. 276, Issue 22, 18653-18656, June 1, 2001
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
276/22/18653    most recent
C100095200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Varrault, A.
Right arrow Articles by Journot, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Varrault, A.
Right arrow Articles by Journot, L.

ACCELERATED PUBLICATION
Characterization of the Methylation-sensitive Promoter of the Imprinted ZAC Gene Supports Its Role in Transient Neonatal Diabetes Mellitus*

Annie VarraultDagger , Benoit Bilanges§, Deborah J. G. Mackay, Eugenia Basyuk||, Barbara Ahr, Céline Fernandez, David O. Robinson, Joël Bockaert, and Laurent Journot

From UPR 9023 CNRS-Centre CNRS-INSERM de Pharmacologie-Endocrinologie-141, rue de la Cardonille, 34094 Montpellier Cedex 05, France and  Wessex Regional Genetics Laboratory, Salisbury District Hospital, Salisbury, Wiltshire SP2 8BJ, United Kingdom

ZAC is a recently isolated zinc finger protein that induces apoptosis and cell cycle arrest. The corresponding gene is imprinted maternally through an unknown mechanism and maps to 6q24-q25, within the minimal interval harboring the gene responsible for transient neonatal diabetes mellitus (TNDM) and a tumor suppressor gene involved in breast cancer. Because of its functional properties, imprinting status, and expression pattern in mammary cell lines and tumors, ZAC is the best candidate so far for both disease conditions. In the present work, we delineated ZAC genomic organization and mapped its transcriptional start site. It is noteworthy that the ZAC promoter localized to the CpG island harboring the methylation imprint associated with TNDM and methylation of this promoter silenced its activity. These data indicate that the methylation mark may have a direct effect on the silencing of the ZAC imprinted allele. Our findings further strengthen the hypothesis that ZAC is the gene responsible for TNDM and suggest a novel mechanism for ZAC inactivation in breast tumors.


* This work was supported by grants from the Centre Nationale de la Recherche Scientifique, La Ligue Nationale contre le Cancer, L'Association pour la Recherche contre le Cancer (ARC), the European Commission (QLG3-CT-1999-00602), and Diabetes UK (RD98/0001627).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Recipient of predoctoral fellowships from the Ministère de l'Education Nationale, de la Recherche et de la Technologie and from the ARC.

|| Recipient of postdoctoral fellowships from the Ministère des Affaires Etrangères and the Fondation pour la Recherche Médicale.

Dagger To whom correspondence should be addressed. Tel.: 33-467 142 963; Fax: 33-467 542 432; E-mail: varrault@ccipe.montp.inserm.fr.


Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


This article has been cited by other articles:


Home page
J. Clin. Endocrinol. Metab.Home page
S. Suzuki, Y. Makita, T. Mukai, K. Matsuo, O. Ueda, and K. Fujieda
Molecular Basis of Neonatal Diabetes in Japanese Patients
J. Clin. Endocrinol. Metab., October 1, 2007; 92(10): 3979 - 3985.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
E. M. Valleley, S. F. Cordery, and D. T. Bonthron
Tissue-specific imprinting of the ZAC/PLAGL1 tumour suppressor gene results from variable utilization of monoallelic and biallelic promoters
Hum. Mol. Genet., April 15, 2007; 16(8): 972 - 981.
[Abstract] [Full Text] [PDF]


Home page
J. Med. Genet.Home page
C Diatloff-Zito, A Nicole, G Marcelin, H Labit, E Marquis, C Bellanne-Chantelot, and J J Robert
Genetic and epigenetic defects at the 6q24 imprinted locus in a cohort of 13 patients with transient neonatal diabetes: new hypothesis raised by the finding of a unique case with hemizygotic deletion in the critical region
J. Med. Genet., January 1, 2007; 44(1): 31 - 37.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
T. Barz, A. Hoffmann, M. Panhuysen, and D. Spengler
Peroxisome Proliferator-Activated Receptor {gamma} Is a Zac Target Gene Mediating Zac Antiproliferation
Cancer Res., December 15, 2006; 66(24): 11975 - 11982.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
A. Hoffmann, T. Barz, and D. Spengler
Multitasking C2H2 Zinc Fingers Link Zac DNA Binding to Coordinated Regulation of p300-Histone Acetyltransferase Activity.
Mol. Cell. Biol., July 1, 2006; 26(14): 5544 - 5557.
[Abstract] [Full Text] [PDF]


Home page
Mol Cancer ResHome page
E. Basyuk, V. Coulon, A. Le Digarcher, M. Coisy-Quivy, J.-P. Moles, A. Gandarillas, and L. Journot
The Candidate Tumor Suppressor Gene ZAC Is Involved in Keratinocyte Differentiation and Its Expression Is Lost in Basal Cell Carcinomas
Mol. Cancer Res., September 1, 2005; 3(9): 483 - 492.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
A. Abdollahi, D. Pisarcik, D. Roberts, J. Weinstein, P. Cairns, and T. C. Hamilton
LOT1 (PLAGL1/ZAC1), the Candidate Tumor Suppressor Gene at Chromosome 6q24-25, Is Epigenetically Regulated in Cancer
J. Biol. Chem., February 14, 2003; 278(8): 6041 - 6049.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
A. Hoffmann, E. Ciani, J. Boeckardt, F. Holsboer, L. Journot, and D. Spengler
Transcriptional Activities of the Zinc Finger Protein Zac Are Differentially Controlled by DNA Binding
Mol. Cell. Biol., February 1, 2003; 23(3): 988 - 1003.
[Abstract] [Full Text]


Home page
J. Med. Genet.Home page
I K Temple and J P H Shield
Transient neonatal diabetes, a disorder of imprinting
J. Med. Genet., December 1, 2002; 39(12): 872 - 875.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.