| Literature DB >> 27604558 |
Sara Benito-Sanz1,2,3, Alberta Belinchon-Martínez1,2,3, Miriam Aza-Carmona1,2,3, Carolina de la Torre1, Celine Huber4, Isabel González-Casado3,5, Judith L Ross6, N Simon Thomas7, Andrew R Zinn8, Valerie Cormier-Daire4, Karen E Heath1,2,3.
Abstract
Short stature homeobox gene (SHOX) is located in the pseudoautosomal region 1 of the sex chromosomes. It encodes a transcription factor implicated in the skeletal growth. Point mutations, deletions or duplications of SHOX or its transcriptional regulatory elements are associated with two skeletal dysplasias, Léri-Weill dyschondrosteosis (LWD) and Langer mesomelic dysplasia (LMD), as well as in a small proportion of idiopathic short stature (ISS) individuals. We have identified a total of 15 partial SHOX deletions and 13 partial SHOX duplications in LWD, LMD and ISS patients referred for routine SHOX diagnostics during a 10 year period (2004-2014). Subsequently, we characterized these alterations using MLPA (multiplex ligation-dependent probe amplification assay), fine-tiling array CGH (comparative genomic hybridation) and breakpoint PCR. Nearly half of the alterations have a distal or proximal breakpoint in intron 3. Evaluation of our data and that in the literature reveals that although partial deletions and duplications only account for a small fraction of SHOX alterations, intron 3 appears to be a breakpoint hotspot, with alterations arising by non-allelic homologous recombination, non-homologous end joining or other complex mechanisms.Entities:
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Year: 2016 PMID: 27604558 DOI: 10.1038/jhg.2016.113
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172