The inheritance of Angelman's syndrome, a disorder characterised by mental retardation, epilepsy, ataxia, and a happy disposition, is debated because affected sibs occur less frequently than expected with autosomal recessive inheritance. After discovering two unrelated patients with a small deletion of the proximal long arm of chromosome 15, 10 further patients with Angelman's syndrome were reassessed. Five had apparently normal karyotypes, four had a deletion within 15q11-13, and one had a pericentric inversion, inv(15)(p11q13) involving the same chromosomal region. In the latter case, the healthy mother had the same pericentric inversion, indicating that the patient also had a submicroscopic mutation on his other chromosome 15. These data map the Angelman locus to 15q11-13 and suggest that de novo visible deletions (associated with a low recurrence risk) and autosomal recessively inherited cases combine to give an overall sib recurrence risk of less than 25%.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1015553PMC
http://dx.doi.org/10.1136/jmg.26.2.73DOI Listing

Publication Analysis

Top Keywords

angelman's syndrome
12
pericentric inversion
8
recurrence risk
8
association angelman's
4
syndrome deletions
4
deletions 15q11-13
4
15q11-13 inheritance
4
inheritance angelman's
4
syndrome disorder
4
disorder characterised
4

Similar Publications

The ubiquitin (Ub) ligase E6AP, which is encoded by the UBE3A gene, has been associated with several human diseases including cervical cancer and Angelman syndrome, a neurodevelopmental disorder. Yet, our knowledge about disease-relevant substrates of E6AP is still limited. The formation of a thioester complex between Ub and the catalytic Cys residue of E6AP represents an essential intermediate step in E6AP-mediated ubiquitination.

View Article and Find Full Text PDF

Gait disturbance is a common motor symptom in Angelman syndrome (AS), but its characteristics have been poorly studied quantitatively. This study aimed to analyze gait characteristics in school-age children with AS using three-dimensional gait analysis (3DGA). Patients with clinically and genetically confirmed AS and healthy children aged 6-15 years were included.

View Article and Find Full Text PDF

Clinical and Cytogenetic Impact of Maternal Balanced Double Translocation: A Familial Case of 15q11.2 Microduplication and Microdeletion Syndromes with Genetic Counselling Implications.

Genes (Basel)

November 2024

Laboratório de Citogenética Clínica, Centro de Genética Médica, Instituto Nacional da Saúde da Mulher, da Criança e do Adolescente Fernandes Figueira-Fundação Oswaldo Cruz, Rio de Janeiro 22250-020, Brazil.

Background: Balanced chromosomal translocations occur in approximately 0.16 to 0.20% of live births.

View Article and Find Full Text PDF

Concordance of Whole-Genome Long-Read Sequencing with Standard Clinical Testing for Prader-Willi and Angelman Syndromes.

J Mol Diagn

January 2025

Department of Laboratory Medicine and Pathology, University of Washington and Seattle Children's Hospital, Seattle, Washington; Division of Genetic Medicine, Department of Pediatrics, University of Washington and Seattle Children's Hospital, Seattle, Washington; Department of Genome Sciences, University of Washington, Seattle, Washington; Brotman Baty Institute for Precision Medicine, University of Washington, Seattle, Washington. Electronic address:

Article Synopsis
  • Current clinical testing for imprinting disorders is complicated and usually involves several tests to get a clear diagnosis.
  • We explored the use of whole-genome long-read sequencing (LRS) as a single test to analyze different genetic variations and methylation patterns in individuals with Prader-Willi or Angelman syndrome.
  • Our results showed that LRS can accurately diagnose these conditions efficiently and could simplify testing while lowering costs and speeding up results in clinical settings.
View Article and Find Full Text PDF

Differences in structure, dynamics and Zn-coordination between isoforms of human ubiquitin ligase UBE3A.

J Biol Chem

December 2024

Department of Molecular Biology and Biophysics, UCONN Health, Farmington, CT 06032, USA. Electronic address:

Article Synopsis
  • UBE3A/E6AP expression abnormalities are linked to neurological disorders like Angelman syndrome and autism, with three protein isoforms existing that have unique functions and cellular roles.
  • Research shows the isoforms differ structurally, particularly in their N-terminal regions, affecting their ability to bind to the proteasome and multimerize, which is crucial for their proper activation.
  • Advanced techniques, including NMR spectroscopy, reveal that some isoforms have dynamic features that could influence their response to oxidative stress, enhancing the understanding of UBE3A's functions and potential therapeutic targets for related disorders.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!