A Requirement for Zic2 in the Regulation of Nodal Expression Underlies the Establishment of Left-Sided Identity
Author:
Funder
British Heart Foundation (BHF)
Wellcome Trust
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-018-28714-1.pdf
Reference73 articles.
1. Brown, S. A. et al. Holoprosencephaly due to mutations in ZIC2, a homologue of Drosophila odd-paired. Nat Genet 20, 180–183, https://doi.org/10.1038/2484 (1998).
2. Solomon, B. D. et al. Mutations in ZIC2 in human holoprosencephaly: description of a novel ZIC2 specific phenotype and comprehensive analysis of 157 individuals. J Med Genet 47, 513–524, https://doi.org/10.1136/jmg.2009.073049 (2010).
3. Mercier, S. et al. New findings for phenotype-genotype correlations in a large European series of holoprosencephaly cases. J Med Genet 48, 752–760, https://doi.org/10.1136/jmedgenet-2011-100339 (2011).
4. Warr, N. et al. Zic2-associated holoprosencephaly is caused by a transient defect in the organizer region during gastrulation. Hum Mol Genet 17, 2986–2996, https://doi.org/10.1093/hmg/ddn197 (2008).
5. Nagai, T. et al. Zic2 regulates the kinetics of neurulation. Proc Natl Acad Sci USA 97, 1618–1623 (2000).
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