Project description:Transcriptional profiling of mouse 3T3-L1 adipocytes. The objective of this study is to explore gene expression profiles of 3T3-L1 adipocytes in response to GDE5 siRNA transfection.
Project description:Insulin is a potent regulator of protein metabolism. Here we describe a time-resolved map of insulin-regulated protein turnover in 3T3-L1 adipocytes using metabolic pulse-chase labelling and high-resolution mass spectrometry.
Project description:3T3-L1 fibroblasts are a commonly used in vitro model for adipogenesis. When induced with hormones, they differentiate into mature fat cells. Here, microarrays were used to study 3T3-L1 adipose differentiation through time. Keywords: time course
Project description:Purpose: The goals of this study are to compare NGS-derived 3T3-L1-NC transcriptome profiling (RNA-seq) to LIGHT overexpression 3T3-L1 cells and find out the DEGs Methods: mRNA profiles of 3T3-L1-NC and 3T3-L1-LIGHT before and after differentiation into beige adipocytes were generated by deep sequencing, in triplicate, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level. Results: Using an optimized data analysis workflow, we mapped about 6.53 Gb data per sample. The average genome mapping rate is 87.27% and the average gene mapping rate is 80.18%. 18,255 genes were identified in which 17,367 of them are known genes and 1,001 of them are novel genes. 13,086 novel transcipts were identified in which 9,304 of them are previously unknown splicing event for known genes, 1,001 of them are novel coding transcripts without any known features, and the remaining 2,781 are long noncoding RNA. Conclusions: Our study represents the first detailed analysis of the impact of LIGHT on gene expression in process of beige adipocytes biogenesis with biologic replicates, generated by RNA-seq technology.
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.
Project description:Target genes of Fbxl10 during 3T3-L1 adipogenesis was analyzed 3T3-L1 cells overexpressing Fbxl10 using retrovirus system containing LTR promoter were differentiated and RNA was extracted at day 2 of differentiation