Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA321980 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Lysine-specific demethylase 1 target genes in brown adipocytes
| PRJNA321978 | ENA
Project description:We performed ChIP-seq to chart genome-wide maps of H3K27me3 in brown preadipocytes and mature brown adipocytes. We observed a subset of brown fat-specific genes, but not common fat genes or white fat-specific genes, possess the H3K27me3 mark in preadipocytes, and this mark is erased in mature adipocytes. H3K27me3 ChIP-seq in brown preadipocytes and mature adipocytes.
2015-12-31 | E-GEOD-55469 | biostudies-arrayexpress
Project description:By screening a collection of epigenetic compounds, we find that Lysine-Specific Demethylase 1 (LSD1) inhibitors repress brown adipocyte differentiation. RNAi-mediated Lsd1 knockdown shows similar effect, which can be rescued by expression of wild-type, but not catalytically inactive, LSD1. Furthermore, adenoviral Cre-mediated LSD1 deletion in mice leads to inhibition of brown adipogenesis, validating the pivotal role of LSD1 in brown fat development in vivo. LSD1 is a histone H3 demethylase, which selectively removes methyl groups from mono- and di-methylated lysine 4 (H3K4me1 and H3K4me2) under most circumstances, and only from lysine 9 (H3K9me1/2) when bound with androgen receptor (AR) or estrogen receptor (ER). K4 demethylation causes transcription repression, while K9 demethylation may lead to activation of gene transcription. To investigate the target genes of LSD1 during BAT differentiaiton, we performed RNA-seq to profile the gene expression in brown adipocytes treated with DMSO or LSD1 inhibitor 611 (Cpd A) for 6 days, and gene set enrichment analysis (GSEA) was then employed to identify Gene Ontology (GO) terms that were significantly enriched.
2016-08-30 | GSE74900 | GEO
Project description:We performed ChIP-seq to chart genome-wide maps of H3K27me3 in brown preadipocytes and mature brown adipocytes. We observed a subset of brown fat-specific genes, but not common fat genes or white fat-specific genes, possess the H3K27me3 mark in preadipocytes, and this mark is erased in mature adipocytes.
2015-12-31 | GSE55469 | GEO
Project description:Lysine-specific demethylase 1 controls beige adipogenesis
| PRJNA219405 | ENA
Project description:Ramirez2017 - Human global metabolism in
brown and white adipocytes
Recon 2.1A, an update to Recon 2.1x, is suitable for
quantitatively-realistic results for flux balance analysis in
human metabolism.
This model is described in the article:
Integrating Extracellular
Flux Measurements and Genome-Scale Modeling Reveals Differences
between Brown and White Adipocytes.
Ramirez AK, Lynes MD, Shamsi F, Xue
R, Tseng YH, Kahn CR, Kasif S, Dreyfuss JM.
Cell Rep 2017 Dec; 21(11):
3040-3048
Abstract:
White adipocytes are specialized for energy storage, whereas
brown adipocytes are specialized for energy expenditure.
Explicating this difference can help identify therapeutic
targets for obesity. A common tool to assess metabolic
differences between such cells is the Seahorse Extracellular
Flux (XF) Analyzer, which measures oxygen consumption and media
acidification in the presence of different substrates and
perturbagens. Here, we integrate the Analyzer's metabolic
profile from human white and brown adipocytes with a
genome-scale metabolic model to predict flux differences across
the metabolic map. Predictions matched experimental data for
the metabolite 4-aminobutyrate, the protein ABAT, and the
fluxes for glucose, glutamine, and palmitate. We also uncovered
a difference in how adipocytes dispose of nitrogenous waste,
with brown adipocytes secreting less ammonia and more urea than
white adipocytes. Thus, the method and software we developed
allow for broader metabolic phenotyping and provide a distinct
approach to uncovering metabolic differences.
This model is hosted on
BioModels Database
and identified by:
MODEL1703310000.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
| MODEL1703310000 | BioModels
Project description:Brown adipose tissue (BAT) dissipates chemical energy in the form of heat, as a defense against hypothermia and obesity. Current evidence indicates that brown adipocytes arise from Myf5+-dermotomal precursors through the action of a PRDM16-C/EBP-_ transcriptional complex; however, the underlying mechanisms that determine lineage specification and maintenance of brown adipose cells remain poorly understood. Here we study the role of euchromatic histone-lysine N-methyltransferase 1 (EHMT1), a brown fat-enriched lysine methyltransferase, as an essential enzymatic component of the PRDM16 transcriptional complex and controls brown adipose cell fate. To identify targets and function of EHMT1, we performed genome-wide gene expression profiling of BAT from control mouce (Ehmt1flox/flox), Ehmt1Myf5 KO mouse (Myf5-Cre+/-; Ehmt1flox/flox) and Ehmt1adipo KO mouse (Adipo-Cre+/-; Ehmt1flox/flox). Loss of EHMT1 in Myf5+ lineage causes a near total loss of brown fat characteristics and induces muscle-selective gene program in vivo. In addition, adipose-specific deletion of EHMT1 by Adipo-Cre leads to a marked reduction of the thermogenic and fat oxidation genes.
2013-11-07 | E-MTAB-1704 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) has in recent times been rediscovered in adult humans, and together with work from preclinical models, shown to have the potential of providing a variety of positive metabolic benefits. These include improved insulin sensitivity and reduced susceptibility to obesity and its various co-morbidities. As such, its continued study could offer insights to therapeutically modulate this tissue to improve metabolic health. It has been reported that adipose-specific deletion of the gene for protein kinase D1 (Prkd1) enhances mitochondrial respiration and improves whole-body glucose homeostasis. We sought to determine whether these effects were mediated specifically through brown adipocytes using a Prkd1 brown adipose tissue (BAT) Ucp1-Cre-specific knockout mouse model, Prkd1BKO. We unexpectedly observed that upon both cold exposure and beta-3-AR agonist administration, Prkd1 loss in BAT did not alter canonical thermogenic gene expression or adipocyte morphology. We took an unbiased approach to assess whether other signaling pathways were altered. RNAs from cold-exposed control and Prkd1BKO were subjected to RNA-Seq analysis. These studies revealed that myogenic gene expression is altered in Prkd1BKO BAT after both acute (8 hr) and extended (4 day) cold exposure. Given that brown adipocytes and skeletal myocytes share a common precursor cell lineage expressing myogenic factor 5 (Myf5), these data suggest that loss of Prkd1 in BAT may alter the biology of preadipocytes in this depot. The data presented herein clarify the role of Prkd1 in BAT thermogenesis and present new avenues for the further study of Prkd1 function in BAT.
2023-09-01 | E-MTAB-12170 | biostudies-arrayexpress
Project description:Expression Data from Bone Marrow Progenitor-Derived Adipocytes, White Adipocytes and Brown Adipocytes.
| PRJNA121839 | ENA