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Predictors for OWOB in PWS

ABSTRACT: Predictors for OWOB in Children with Prader Willi Syndrome

PROVIDER: PRJEB34398 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3518520_1.fastq.gz	Fastqsanger.gz
	ERR3518520_2.fastq.gz	Fastqsanger.gz
	ERR3518530_1.fastq.gz	Fastqsanger.gz
	ERR3518530_2.fastq.gz	Fastqsanger.gz
	ERR3518540_1.fastq.gz	Fastqsanger.gz

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Predictors for OWOB in PWS

Project description:Predictors for OWOB in Children with Prader Willi Syndrome

| PRJEB34398 | ENA

Predictors for OWOB in children with Prader Willi Syndrome

Project description:Predictors for OWOB in children with Prader Willi Syndrome

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Insulin secretion deficits in a Prader-Willi syndrome β-cell model are associated with a concerted downregulation of multiple endoplasmic reticulum chaperones [ncRNA-Seq]

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Insulin secretion deficits in a Prader-Willi syndrome β-cell model are associated with a concerted downregulation of multiple endoplasmic reticulum chaperones [RNA-seq]

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Differential Gene Expression and Mitochondrial Dysfunction in Imprinting center deletion (PWS- IC del) Mouse model of Prader-Willi Syndrome

Project description:Prader-Willi syndrome (PWS) is a genetic disorder caused by deficiency of imprinted gene expression from the paternal chromosome 15q11-15q13 and clinically characterized by neonatal hypotonia, short stature, cognitive impairment, hypogonadism, hyperphagia, morbid obesity and diabetes. Previous clinical studies suggest that a defect in energy metabolism may be involved in the pathogenesis of PWS. Assessment of enzyme activities of mitochondrial oxidative phosphorylation (OXPHOS) complexes in the brain, heart, liver and muscle were assessed. We used microarrays to detail the global programme of gene expression underlyingthe PWS and identified distinct classes of disregulated genes during this process. Skeletal (quadriceps) muscle Vastus Lateralis and whole brain samples from the mutant mice and their wild-type age-matched littermates were analyzed by microarray technology using the Mouse Genome 430 2.0 arrays (Affymetrix).

2013-04-19 | E-GEOD-41759 | biostudies-arrayexpress

Differential Gene Expression and Mitochondrial Dysfunction in Imprinting center deletion (PWS- IC del) Mouse model of Prader-Willi Syndrome

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Transcriptomic response to 24-hour food deprivation in four hypothalamic nuclei in Snord116 deletion mice

Project description:Mice with a congenital Snord116 deletion model aspects of the Prader-Willi Syndrome. In this study, we examine the gene expression changes in four hypothalamic nuclei across 24-hour food deprived versus ad libitum fed mice.

2017-12-31 | GSE102992 | GEO

Transcriptomic response to adult hypothalamic deletion of Snord116

Project description:Snord116 deletion mouse models recapitulate aspects of the Prader-Willi Syndrome. In this study, we examine the gene expression changes in the mediobasal hypothalamus for mice which have an adult onset deletion of Snord116 in the mediobasal hypothalamus.

2017-12-31 | GSE106210 | GEO

Prader-Willi Syndrome Microbiota

Project description:Prader-Willi Syndrome Microbiota Targeted loci environmental

| PRJNA669563 | ENA

The noncoding RNA IPW regulates the imprinted DLK1-DIO3 locus in an induced pluripotent stem cell model of Prader-Willi syndrome

Project description:Parental imprinting is a form of epigenetic regulation that results in parent-of-origin differential gene expression. To study Prader-Willi syndrome (PWS), a developmental imprinting disorder, we generated patient-derived induced pluripotent stem cells (iPSCs) harboring distinct deletions in the affected region on chromosome 15. Studying PWS-iPSCs and human parthenogenetic iPSCs unexpectedly revealed substantial upregulation of virtually all maternally expressed genes (MEGs) in the imprinted DLK1-DIO3 locus on chromosome 14. Subsequently, we identified IPW, a long noncoding RNA in the critical region of the PWS locus, as a regulator of the DLK1-DIO3 region, as its over-expression in PWS and parthenogenetic iPSCs results in downregulation of the MEGs in this locus. We further show that gene expression changes in the DLK1-DIO3 region coincide with chromatin modifications, rather than DNA methylation levels. Our results suggest that a subset of PWS phenotypes may arise from dysregulation of an imprinted locus distinct from the PWS region. Gene expression analysis was performed on a total of 4 human cell lines, including 3 Prader-Willi Syndrome indcued pluripotent stem cell lines - derived from 3 affected individuals and one of their parental fibroblast cell line.

2014-04-03 | E-GEOD-56136 | biostudies-arrayexpress

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