ArticleGenomics2005
Microarray analysis of gene/transcript expression in Angelman syndrome: deletion versus UPD.
Article in Genomics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Prader-Willi syndrome: a review of clinical, genetic, and endocrine findings.Journal of endocrinological investigation · 2015Review
- Differences between the pattern of developmental abnormalities in autism associated with duplications 15q11.2-q13 and idiopathic autism.Journal of neuropathology and experimental neurology · 2012Article
- 12-year-old boy with a 4q35.2 microdeletion and involvement of MTNR1A, FAT1, and F11 genes.Clinical dysmorphology · 2012Article
- Genetic variants and monoallelic expression of surfactant protein-D in inflammatory bowel disease.Annals of human genetics · 2011Article
- Gene expression in cardiac tissues from infants with idiopathic conotruncal defects.BMC medical genomics · 2011Article
- Somatosensory and sensorimotor consequences associated with the heterozygous disruption of the autism candidate gene, Gabrb3.Behavioural brain research · 2011Article
- Methylation profiling in individuals with uniparental disomy identifies novel differentially methylated regions on chromosome 15.Genome research · 2010Article
- Analysis of the Prader-Willi syndrome chromosome region using quantitative microsphere hybridization (QMH) array.American journal of medical genetics. Part A · 2008Article
- Immunologic and neurodevelopmental susceptibilities of autism.Neurotoxicology · 2008Review
- 15q11-13 GABAA receptor genes are normally biallelically expressed in brain yet are subject to epigenetic dysregulation in autism-spectrum disorders.Human molecular genetics · 2007Article
- Whole genome microarray analysis of gene expression in an imprinting center deletion mouse model of Prader-Willi syndrome.American journal of medical genetics. Part A · 2007Article
- Whole genome microarray analysis of gene expression in Prader-Willi syndrome.American journal of medical genetics. Part A · 2007Article
- Prader-Willi syndrome: clinical genetics, cytogenetics and molecular biology.Expert reviews in molecular medicine · 2005Review
- Coding and noncoding expression patterns associated with rare obesity-related disorders: Prader-Willi and Alström syndromes.Advances in genomics and geneticsArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Angelman syndrome (AS) is a neurodevelopmental disorder due to a functional deficit, usually a deletion, of the UBE3A gene located in the 15q11-q13 chromosome region. We report the first microarray analysis of gene expression in AS using a custom cDNA microarray to compare expression patterns from lymphoblastoid cell lines from control males and AS subjects with a 15q deletion or uniparental paternal disomy 15. Expression patterns of genes known to be biallelically expressed or paternally or maternally expressed were consistent with expectations. We detected paternal or maternal allelic bias in the expression of several genes and transcripts (e.g., GABRA5, GABRB3, WI-14946). Additionally, mechanisms controlling paternal allele expression appear to be faithfully replicated in each paternal chromosome in individuals with paternal disomy. Our results indicate that interconnected mechanisms can produce subtle and unexpected changes in gene expression that may help explain the phenotypic differences observed among the genetic subtypes of AS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.