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Hi-C analysis of day 0 3T3-L1 cells transfected with scrambled and Prmt5 siRNA

ABSTRACT: Hi-C analysis of day 0 3T3-L1 cells transfected with scrambled and Prmt5 siRNA

PROVIDER: PRJNA794127 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17425759_1.fastq.gz	Fastqsanger.gz
	SRR17425759_2.fastq.gz	Fastqsanger.gz
	SRR17425760_1.fastq.gz	Fastqsanger.gz
	SRR17425760_2.fastq.gz	Fastqsanger.gz
	SRR17425761_1.fastq.gz	Fastqsanger.gz

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Hi-C analysis of day 0 3T3-L1 cells transfected with scrambled and Prmt5 siRNA

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Transcriptome analysis of day 0 3T3-L1 cells transfected with scrambled and Prmt5 siRNA

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Transcriptome analysis of day 0 3T3-L1 cells transfected with scrambled and Prmt5 siRNA

Project description:Transcriptome analysis of day 0 3T3-L1 cells transfected with scrambled and Prmt5 siRNA

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Genome-wide profiling of Prmt5 binding during 3T3-L1 adipogenesis

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LSD1 knockdown in 3T3-L1 preadipocytes

Project description:Obesity is often associated with a low-grade systemic inflammation state that contributes to the development of insulin resistance and atherosclerotic complications. This is usually coupled with increased macrophage infiltration in the adipose tissue and a defect in adipocyte differentiation that results in accumulation of hypertrophic fat cells characterized by a deregulated pattern of adipokine expression. Here we show that knockdown of histone demethylase lsd1 in 3T3-L1 preadipocytes results in defective adipogenesis and derepression of an inflammatory program in these cells. The dataset consists of four sample groups: [1] 3T3-L1 preadipocytes (passage 19) transfected with a control scrambled siRNA at 24h after transfection (siC.24h), [2] 3T3-L1 preadipocytes (p.19) transfected with a siRNA directed against LSD1 at 24h after transfection (siLsd1.24h), [3] 3T3-L1 preadipocytes (p.21) transfected with a control scrambled siRNA at 48h after transfection (siC.48h), and [4] 3T3-L1 preadipocytes (p.21) transfected with a siRNA directed against LSD1 at 48h after transfection (siLsd1.48h). The 24h sample groups (siC.24h and siLsd1.24h) consist of two biological replicate samples; the 48h sample groups (siC.48h and siLsd1.48h) consist of three biological replicate samples. Each sample was hybridized to a separate array, for a total of ten arrays.

2013-12-31 | E-GEOD-25423 | biostudies-arrayexpress

Methylation profiling of 3T3-L1 Cells: Control vs slincRAD-shRNA8 stable transfected

Project description:Genome-wide methylation profiling of mouse 3T3-L1 Cells comparing control wildtypes with cells stable transfected with slincRAD shRNA8 (sh8).

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Methylation profiling of 3T3-L1 Cells: Control vs slincRAD-shRNA8 stable transfected

Project description:Genome-wide methylation profiling of mouse 3T3-L1 Cells comparing control wildtypes with cells stable transfected with slincRAD shRNA8 (sh8). Two-condition experiment, 3T3-L1 wildtype vs. slincRAD-shRNA8 stable transfected cells before and after Adipogenesis. One replicate per array.

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Genome-wide profiling of Prmt5 binding during 3T3-L1 adipogenesis

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Differentiating 3T3-L1 adipocytes, introduced with siRNA against phf21a gene

Project description:Adipogenic differentiation and metabolic adaptation are initiated through transcriptional and epigenetic reprogramming. In particular, dynamic changes in histone modifications may play central roles in the rearrangement of gene expression patterns. BHC80 protein, encoded by phf21a gene, is a part of LSD1 histone demethylase complex and is essential for the demethylation activity. To address the importance of histone demethylation in adipogenic differentiation and function, we performed cDNA microarray in BHC80-deficient 3T3-L1 cells 3T3-L1 preadipocytes were transfected with either BHC80-specific siRNA or control siRNA (siGL3). 24 hours later, cells were subjected to adipogenic induction. 24 hours later, cells were harvested for total RNA extraction.

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