The following are links to data we’ve published in the last 5 years. Click here to see all published data sets.
Warming Induces Significant Reprogramming of Beige, but Not Brown, Adipocyte Cellular Identity
Design: Ucp1-NuTRAP and Adipoq-NuTRAP mice exposed to different temperatures were used for brown, beige or white adipocyte-specific transcriptomic and epigenomic analysis.
Organism: Mus musculus
Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
58 Samples
Citation for this data set:
Roh HC, Tsai LTY, Shao M, Tenen D et al. Warming Induces Significant Reprogramming of Beige, but Not Brown, Adipocyte Cellular Identity. Cell Metab 2018 May 1;27(5):1121-1137.e5. PMID: 29657031
Transcriptional profile of brown adipose tissue (BAT) and white vastus lateralis (WV) from BATI4KO mice
Design: We report RNA-seq data from the brown fat and vastus muscles of mice lacking IRF4 in brown fat (BATI4KO) vs floxed littermate controls
Organism: Mus musculus
Type: Expression profiling by high throughput sequencing
21 Samples
Simultaneous transcriptional and epigenomic profiling from specific cell types within heterogeneous tissues in vivo
Design: Using NuTRAP, we successfully characterize gene expression and epigenomic states of various adipocyte populations in vivo. To demonstrate general usefulness, we chateraterize histone states of in vivo hepatocytes.
Organism: Mus musculus
Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
36 Samples
Citation for this data set:
Roh HC, Tsai LT, Lyubetskaya A, Tenen D et al. Simultaneous Transcriptional and Epigenomic Profiling from Specific Cell Types within Heterogeneous Tissues In Vivo. Cell Rep 2017 Jan 24;18(4):1048-1061. PMID: 28122230
Characterising the transcriptional profile of murine 3T3-L1 adipocytes with altered expression of IRF3
Design: Transcriptional profiling of murine 3T3-L1 adipocytes with altered expression of IRF3. Overexpression or knockdown of IRF3 was achieved by lentivirus transduction for 6 days. 3T3-L1 adipocytes with IRF3 knockdown were further treated in the absence or presence of LPS for 6 days. Samples consist of triplicate replica with appropriate control.
Organism: Mus musculus
Type: Expression profiling by high throughput sequencing
18 Samples
Citation for this data set:
Kumari M, Wang X, Lantier L, Lyubetskaya A et al. IRF3 promotes adipose inflammation and insulin resistance and represses browning. J Clin Invest 2016 Aug 1;126(8):2839-54. PMID: 27400129
Transcriptional responses of mouse adipocytes during insulin resistance
Design: Murine 3T3-L1 adipocytes were treated separately with dexamethasone (Dex; 20nM) or tumor necrosis factor-alpha. To comprehensively assess gene expression changes caused by Dex and TNF in a time-dependent manner, we profiled cells at early (2 hours), intermediate (24 hours), and late (6 days) points in the development of insulin resistance.
Organism: Mus musculus
Type: Expression profiling by array
21 Samples
Citation for this dataset:
Kang S, Tsai LT, Zhou Y, Evertts A et al. Identification of nuclear hormone receptor pathways causing insulin resistance by transcriptional and epigenomic analysis. Nat Cell Biol 2015 Jan;17(1):44-56. PMID: 25503565
Characterizing the profiles of histone markers in mouse adipocytes during insulin resistance
Design: Murine 3T3-L1 adipocytes were treated separately with dexamethasone (Dex; 20nM) or tumor necrosis factor-alpha. To comprehensively assess gene expression changes caused by Dex and TNF in a time-dependent manner, we profiled cells at early (2 hours), intermediate (24 hours), and late (6 days) points in the development of insulin resistance.
Organism: Mus musculus
Type: Genome binding/occupancy profiling by high throughput sequencing
66 Samples
Citation for this dataset:
Kang S, Tsai LT, Zhou Y, Evertts A et al. Identification of nuclear hormone receptor pathways causing insulin resistance by transcriptional and epigenomic analysis. Nat Cell Biol 2015 Jan;17(1):44-56. PMID: 25503565