Inter- and Intrachromosomal Rearrangements Are Both Involved in the Origin of 15q11-q13 Deletions in Prader-Willi Syndrome
- 1 July 1997
- journal article
- Published by Elsevier in American Journal of Human Genetics
- Vol. 61 (1), 228-231
- https://doi.org/10.1086/513907
Abstract
No abstract availableThis publication has 17 references indexed in Scilit:
- Unequal interchromosomal rearrangements may result in elastin gene deletions causing the Williams-Beuren syndromeHuman Molecular Genetics, 1996
- A recombination hotspot responsible for two inherited peripheral neuropathies is located near a mariner transposon-like elementNature Genetics, 1996
- An STS-Based Map of the Human GenomeScience, 1995
- Factor VIII gene inversions causing severe hemophilia A originate almost exclusively in male germ cellsHuman Molecular Genetics, 1994
- Two autosomal dominant neuropathies result from reciprocal DNA duplication/deletion of a region on chromosome 17Human Molecular Genetics, 1994
- Inversions disrupting the factor VIII gene are a common cause of severe haemophilia ANature Genetics, 1993
- Duplication of chromosome 15 in the region 15q11-13 in a patient with developmental delay and ataxia with similarities to Angelman syndrome.Journal of Medical Genetics, 1993
- Cytogenetic and molecular studies in the Prader-Willi and Angelman syndromes: An overviewAmerican Journal of Medical Genetics, 1993
- Charcot–Marie–Tooth type 1A duplication appears to arise from recombination at repeat sequences flanking the 1.5 Mb monomer unitNature Genetics, 1992
- Duplication of seven exons in LDL receptor gene caused by Alu-Alu recombination in a subject with familial hypercholesterolemiaCell, 1987