Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (37)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Roberts, C.
Right arrow Articles by Scambler, P. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Roberts, C.
Right arrow Articles by Scambler, P. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Molecular Genetics, Vol 6, 237-245, Copyright © 1997 by Oxford University Press

ARTICLES

Cloning and developmental expression analysis of chick Hira (Chira), a candidate gene for DiGeorge syndrome

C Roberts, SC Daw, S Halford and PJ Scambler
Molecular Medicine Unit, Institute of Child Health, London, UK.

Deletions within human chromosome 22q11 cause a wide variety of birth defects including the DiGeorge syndrome and velo-cardio-facial (Shprintzen) syndrome. Despite the positional cloning of several genes from the critical region, it is still not possible to state whether the phenotype is secondary to haploinsufficiency of one or more than one gene. In embryological studies phenocopies of these abnormalities are produced by a variety of actions which disrupt the contribution made by the cranial and cardiac neural crest to development. The TUPLE1/HIRA gene is related to WD40 domain transcriptional regulators and maps within the DiGeorge critical region. We have cloned the chick homologue of HIRA and conducted in situ expression analysis in early chick embryos. Hira is expressed in the developing neural plate, the neural tube, neural crest and the mesenchyme of the head and branchial arch structures. HIRA may therefore have a role in the haploinsufficiency syndromes caused by deletion of 22q11.
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
 Cereb CortexHome page
C. E. Bearden, T. G.M. van Erp, R. A. Dutton, H. Tran, L. Zimmermann, D. Sun, J. A. Geaga, T. J. Simon, D. C. Glahn, T. D. Cannon, et al.
Mapping Cortical Thickness in Children with 22q11.2 Deletions
Cereb Cortex, August 1, 2007; 17(8): 1889 - 1898.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Greenall, E. S. Williams, K. A. Martin, J. M. Palmer, J. Gray, C. Liu, and S. K. Whitehall
Hip3 Interacts with the HIRA Proteins Hip1 and Slm9 and Is Required for Transcriptional Silencing and Accurate Chromosome Segregation
J. Biol. Chem., March 31, 2006; 281(13): 8732 - 8739.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Ahmad, H. Kikuchi, Y. Takami, and T. Nakayama
Different Roles of N-terminal and C-terminal Halves of HIRA in Transcription Regulation of Cell Cycle-related Genes That Contribute to Control of Vertebrate Cell Growth
J. Biol. Chem., September 16, 2005; 280(37): 32090 - 32100.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
C. Blackwell, K. A. Martin, A. Greenall, A. Pidoux, R. C. Allshire, and S. K. Whitehall
The Schizosaccharomyces pombe HIRA-Like Protein Hip1 Is Required for the Periodic Expression of Histone Genes and Contributes to the Function of Complex Centromeres
Mol. Cell. Biol., May 15, 2004; 24(10): 4309 - 4320.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
C. Roberts, H. F. Sutherland, H. Farmer, W. Kimber, S. Halford, A. Carey, J. M. Brickman, A. Wynshaw-Boris, and P. J. Scambler
Targeted Mutagenesis of the Hira Gene Results in Gastrulation Defects and Patterning Abnormalities of Mesoendodermal Derivatives Prior to Early Embryonic Lethality
Mol. Cell. Biol., April 1, 2002; 22(7): 2318 - 2328.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
C. Hall, D. M. Nelson, X. Ye, K. Baker, J. A. DeCaprio, S. Seeholzer, M. Lipinski, and P. D. Adams
HIRA, the Human Homologue of Yeast Hir1p and Hir2p, Is a Novel Cyclin-cdk2 Substrate Whose Expression Blocks S-Phase Progression
Mol. Cell. Biol., March 1, 2001; 21(5): 1854 - 1865.
[Abstract] [Full Text]

Home page
 Arch Gen PsychiatryHome page
S. Eliez, S. E. Antonarakis, M. A. Morris, S. P. Dahoun, and A. L. Reiss
Parental Origin of the Deletion 22q11.2 and Brain Development in Velocardiofacial Syndrome: A Preliminary Study
Arch Gen Psychiatry, January 1, 2001; 58(1): 64 - 68.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
M. J. Farrell, H. Stadt, K. T. Wallis, P. Scambler, R. L. Hixon, R. Wolfe, L. Leatherbury, and M. L. Kirby
HIRA, a DiGeorge Syndrome Candidate Gene, Is Required for Cardiac Outflow Tract Septation
Circ. Res., February 5, 1999; 84(2): 127 - 135.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
S. Lorain, J.-P. Quivy, F. Monier-Gavelle, C. Scamps, Y. Lécluse, G. Almouzni, and M. Lipinski
Core Histones and HIRIP3, a Novel Histone-Binding Protein, Directly Interact with WD Repeat Protein HIRA
Mol. Cell. Biol., September 1, 1998; 18(9): 5546 - 5556.
[Abstract] [Full Text]


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.