Skip Navigation



Human Molecular Genetics Advance Access published online on August 7, 2006
Human Molecular Genetics, doi:10.1093/hmg/ddl209
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
15/18/2732    most recent
ddl209v1
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Hung, M.-S.
Right arrow Articles by Rogner, U. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hung, M.-S.
Right arrow Articles by Rogner, U. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press. All rights reserved
Received July 3, 2006
Accepted July 31, 2006

Article

Identification of the transcription factor Arntl2 as a candidate gene for the type 1 diabetes locus Idd6

Ming-Shiu Hung 1, Philip Avner 1, and Ute Christine Rogner 1 *

1 Unité de Génétique Moléculaire Murine CNRS URA 2578, Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15

* To whom correspondence should be addressed.
Ute Christine Rogner, E-mail: urogner{at}pasteur.fr


  Abstract

The Idd6 murine type 1 diabetes locus has been shown to control diabetes by regulating the protective activity of the peripheral immune system as demonstrated by diabetes transfer assays using splenocytes. The analysis of three novel subcongenic NOD.C3H strains has confirmed the presence of at least two diabetes related genes within the 5.8 Mb Idd6 interval with the disease protection conferred by splenocyte co-transfer being located to the 700 kb Idd6.3 subregion. This sub-interval contains the circadian rhythm related transcription factor Arntl2 (Bmal2), a homologue of the type 2 diabetes associated ARNT (HIF1ß) gene. Arntl2 exhibited a six-fold upregulation in spleens of the NOD.C3H 6.VIII congenic strain compared to the NOD control strain, strain-specific splice variants and a large number of polymorphisms in both coding and non-coding regions. Arntl2 upregulation was not associated with changes in the expression levels of other circadian genes in the spleen, but did correlate with the upregulation of the ARNT-binding motif containing Pla2g4a gene, that has recently been described as being protective for the progression of insulitis and autoimmune diabetes in the NOD mouse via regulation of the TNFalpha pathway. Our studies strongly suggest that the HIFß-homologous Arntl2 gene is involved in the control of type 1 diabetes.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Immunol.Home page
D. Vallois, M.-C. Gagnerault, P. Avner, U. C. Rogner, C. Boitard, K. Benlagha, A. Herbelin, and F. Lepault
Influence of a Non-NK Complex Region of Chromosome 6 on CD4+ Invariant NK T Cell Homeostasis
J. Immunol., August 1, 2008; 181(3): 1753 - 1759.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
V. Dror, T. B. Kalynyak, Y. Bychkivska, M. H. Z. Frey, M. Tee, K. D. Jeffrey, V. Nguyen, D. S. Luciani, and J. D. Johnson
Glucose and Endoplasmic Reticulum Calcium Channels Regulate HIF-1{beta} via Presenilin in Pancreatic {beta}-Cells
J. Biol. Chem., April 11, 2008; 283(15): 9909 - 9916.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
D. Vallois, C. H. Grimm, P. Avner, C. Boitard, and U. C. Rogner
The Type 1 Diabetes Locus Idd6 Controls TLR1 Expression
J. Immunol., September 15, 2007; 179(6): 3896 - 3903.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.