ArticleJournal of medical genetics2003
Microarray analysis of gene/transcript expression in Prader-Willi syndrome: deletion versus UPD.
Article in Journal of medical genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 61 citations in OpenAlex.
- Prader-Willi syndrome, deletion subtypes, and magnesium: Potential impact on clinical findings.American journal of medical genetics. Part A · 2022Article
- Health Problems in Adults with Prader-Willi Syndrome of Different Genetic Subtypes: Cohort Study, Meta-Analysis and Review of the Literature.Journal of clinical medicine · 2022Article
- Parent-of-Origin Effects in 15q11.2 BP1-BP2 Microdeletion (Burnside-Butler) Syndrome.International journal of molecular sciences · 2019Article
- Preliminary observations of mitochondrial dysfunction in Prader-Willi syndrome.American journal of medical genetics. Part A · 2018Article
- Benefits and limitations of prenatal screening for Prader-Willi syndrome.Prenatal diagnosis · 2017Review
- Prader-Willi syndrome: a review of clinical, genetic, and endocrine findings.Journal of endocrinological investigation · 2015Review
- Differential gene expression reveals mitochondrial dysfunction in an imprinting center deletion mouse model of Prader-Willi syndrome.Clinical and translational science · 2013Article
- 12-year-old boy with a 4q35.2 microdeletion and involvement of MTNR1A, FAT1, and F11 genes.Clinical dysmorphology · 2012Article
- Prader-Willi Syndrome: Obesity due to Genomic Imprinting.Current genomics · 2011Article
- Somatosensory and sensorimotor consequences associated with the heterozygous disruption of the autism candidate gene, Gabrb3.Behavioural brain research · 2011Article
- Genetic subtype differences in neural circuitry of food motivation in Prader-Willi syndrome.International journal of obesity (2005) · 2009Article
- Gender influences monoallelic expression of ATP10A in human brain.Human genetics · 2008Article
- Analysis of the Prader-Willi syndrome chromosome region using quantitative microsphere hybridization (QMH) array.American journal of medical genetics. Part A · 2008Article
- Top-down or bottom-up: Contrasting perspectives on psychiatric diagnoses.Biologics : targets & therapy · 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
- X-chromosome inactivation patterns in females with 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
- 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
- A 9-year-old male with a duplication of chromosome 3p25.3p26.2: clinical report and gene expression analysis.American journal of medical genetics. Part A · 2006Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPrader-Willi syndrome (PWS), the most common genetic cause of marked obesity, is caused by genomic imprinting and loss of expression of paternal genes in the 15q11-q13 region. There is a paucity of data examining simultaneous gene expression in this syndrome.
methodsWe generated cDNA microarrays representing 73 non-redundant genes/transcripts from the 15q11-q13 region, the majority within the PWS critical region and others distally on chromosome 15. We used our custom microarrays to compare gene expression from actively growing lymphoblastoid cell lines established from nine young adult males (six with PWS (three with deletion and three with UPD) and three controls).
resultsThere was no evidence of expression of genes previously identified as paternally expressed in the PWS cell lines with either deletion or UPD. We detected no difference in expression of genes with known biallelic expression located outside the 15q11-q13 region in all cell lines studied. There was no difference in expression levels of biallelically expressed genes (for example, OCA2) from within 15q11-q13 when comparing UPD cell lines with controls. However, two genes previously identified as maternally expressed (UBE3A and ATP10C) showed a significant increase in expression in UPD cell lines compared with control and PWS deletion subjects. Several genes/transcripts (for example, GABRA5, GABRB3) had increased expression in UPD cell lines compared with deletion, but less than controls indicating paternal bias.
conclusionsOur results suggest that differences in expression of candidate genes may contribute to phenotypic differences between PWS subjects with deletion or UPD and warrant further investigations.
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