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Expression data from Merm1/Wbscr22 knock-down tumor cells

ABSTRACT: Merm1/Wbscr22 is one of genes in chromosomal region deleted in Williams-Beuren syndrome, a multisystem developmental disorder. Wbscr22 contains a nuclear localization signal and an S-adenosyl-L-methionine-dependent methyltransferase fold, but its real function is completely unknown.　In this study, to examine the function, we compared the gene expression profiles between control and Merm1/Wbscr22 knock-downed tumor cells.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE22065 | GEO | 2010/09/01

SECONDARY ACCESSION(S): PRJNA127485

REPOSITORIES: GEO

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Expression data from Merm1/Wbscr22 knock-down tumor cells

Project description:Merm1/Wbscr22 is one of genes in chromosomal region deleted in Williams-Beuren syndrome, a multisystem developmental disorder. Wbscr22 contains a nuclear localization signal and an S-adenosyl-L-methionine-dependent methyltransferase fold, but its real function is completely unknown.　In this study, to examine the function, we compared the gene expression profiles between control and Merm1/Wbscr22 knock-downed tumor cells. Four established cell lines were selected for RNA extraction and hybridization on Affymetrix microarrays: (1) control LM8 cells, designated as LM8/control, (2) Merm1/Wbscr22 knock-downed LM8 cells, designated as LM8/shRNA, (3) control A375M cells, designated as A375M/control, and (4) Merm1/Wbscr22 knock-downed A375M cells, designated as A375M/shRNA.

2010-09-01 | E-GEOD-22065 | biostudies-arrayexpress

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Williams-Beuren syndrome: typical deletions versus atypical deletions of the 7q11.23 region

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The deletion of the Williams-Beuren Syndrome critical region dysregulate the expression of miR379-410 miRNA members in human isogenic iNeurons

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7q11.23 CNV altered proteome in iPSC differentiating neurons

Project description:Copy number variations (CNVs) at 7q11.23 cause Williams-Beuren (WBS) and 7q microduplication syndromes (7Dup), two neurodevelopmental disorders with shared and opposite cognitive-behavioral phenotypes. Using patient-derived and isogenic neurons, we integrated transcriptomics, translatomics and proteomics to elucidate the molecular underpinnings of this dosage effect. We found that 7q11.23 CNVs cause opposite alterations in neuronal differentiation and neuronal excitability. Here, the 7q11.23 CNV altered proteome in iPSC differentiating neurons was measured by a fast SWATH-MS method.

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Next Generation Sequencing Quantitative Analysis of Wild Type and RALY knock-down HCT 116 cells Transcriptomes

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of gene expression and alternative RNA splicing. The goals of this study are to compare alternative splicing in RALY knock-down cells to identify the function of RALY in alternative splicing transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Methods: mRNA profiles of RALY knock-dowed HCT 116 cells and non-silencing shRNA treated HCT 116 cells generated by deep sequencing, in duplicate, using Illumina Hiseq 2500. Results: Using an we mapped about more than 60 million reads per sample to the human genome (GRCh38) and identified 58,884 transcripts in WT and RALY knock-downed HCT 116 cells with Hisat2. rMATS analysis of RNA-seq data demonstrate significant effects of RALY on 4,046 skipped exon splicing and other alternative splicing events. Conclusions: Our study represents the first detailed analysis of transcriptomes in RALY KD cells, with biologic duplicates, generated by RNA-seq technology. The splicing analysis workflows reported here should provide a framework for the RALY function in the splicing.

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