Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-68382

ABSTRACT: Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]

OTHER RELATED OMICS DATASETS IN: PRJNA282719PRJNA282723PRJNA282744PRJNA289018

PROVIDER: E-GEOD-68382 | ExpressionAtlas | 2016-01-08

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-68382-analysis-methods.tsv	Tabular
	E-GEOD-68382-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-68382-configuration.xml	Xml
	E-GEOD-68382-percentile-ranks.tsv	Tabular
	E-GEOD-68382.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 50

Similar Datasets

E-GEOD-68429

Project description:Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]

2016-01-08 | E-GEOD-68429 | ExpressionAtlas

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity

Project description:Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity

| PRJNA282744 | ENA

Mus musculus

Project description:Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]

| PRJNA282723 | ENA

Mus musculus

Project description:Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]

| PRJNA282719 | ENA

Ablation of TET proteins in adipocytes protects against adiposity and metabolic dysfunction by potentiating energy expenditure

Project description:Ten-eleven translocation (TET) proteins oxidize 5-methylcytosine in DNA to 5- hydroxymethylcytosine and further oxidized derivatives. Here we show that TET proteins are key epigenetic suppressors of adipocyte thermogenesis and energy expenditure in both white and brown adipose tissues in vivo. Tet expression in adipocytes decreases upon cold or adrenergic stimulation but increases following high-fat diet (HFD) consumption. Mice with triple deletion of all three Tet genes in adipocytes have higher energy expenditure due to enhanced fat browning and thermogenesis. They also show significantly enhanced lipolysis because of elevated expression of Adrb3 and key lipases including Atgl and Hsl. Consequently, the knockout mice display improved cold tolerance and are substantially resistant to obesity, inflammation, and associated metabolic complications including insulin resistance. Mechanistically, TET deficiency substantially prevents the HFD-induced transcriptional alterations in adipose tissues. TET proteins recruit histone deacetylases (HDACs) to the key thermogenic gene loci including Adrb3, Ppargc1a, and Ucp1, leading to transcriptional repression through histone deacetylation. Thus, the TET-HDAC axis may be therapeutically targeted to treat obesity and related metabolic diseases.

2021-11-01 | GSE178762 | GEO

SOX4 facilitates brown fat development and maintenance through EBF2-mediated thermogenic gene program in mice [ChIP-Seq]

Project description:Brown adipose tissue (BAT) is critical for non-shivering thermogenesis making it a promising therapeutical strategy to combat obesity and metabolic disease. However, the regulatory mechanisms underlying brown fat formation remain incompletely understood. Here, we found SOX4 is required for BAT development and thermogenic program. Depletion of SOX4 in BAT progenitors (Sox4-MKO) or brown adipocytes (Sox4-BKO) resulted in whitened BAT and hypothermia upon acute cold exposure. The reduced thermogenic capacity observed in Sox4-MKO mice increases their susceptibility to diet-induced obesity. Overexpression of SOX4 enhances BAT thermogenesis counteracting diet-induced obesity. Mechanistically, SOX4 activates transcription of EBF2 which determines brown fat fate. Moreover, phosphorylation of SOX4 at S235 by PKA facilitates its nuclear translocation and EBF2 transcription. Further, SOX4 cooperates with EBF2 to activate transcriptional programs governing thermogenic gene expression. These results demonstrate that SOX4 serves as an upstream regulator of EBF2 providing valuable insights into BAT development and thermogenic function maintenance.

2025-03-19 | GSE263446 | GEO

SOX4 facilitates brown fat development and maintenance through EBF2-mediated thermogenic gene program in mice [RNA-Seq]

2025-03-19 | GSE263445 | GEO

Autotaxin and its product lysophosphatidic acid suppress brown adipose differentiation and promote diet-induced obesity in mice

Project description:Brown adipose tissue (BAT) is a thermogenic organ that dissipates stored energy as heat to maintain body temperature in infants and small mammals. This process may also provide protection from development of diet-induced obesity. We found that the bioactive lipid mediator lysophosphatidic acid (LPA) markedly decreases differentiation of cultured primary brown adipocyte precursors, while potent selective inhibitors of the LPA-generating enzyme autotaxin (ATX) promote differentiation. Transgenic mice overexpressing ATX exhibited reduced expression of BAT-related genes in peripheral white adipose tissue and accumulated significantly more fat than wild-type controls when fed a high fat diet. Our results indicate that ATX and its product LPA are physiologically relevant negative regulators of brown fat adipogenesis and suggest that a decrease in peripheral brown adipose tissue results in increased susceptibility to diet-induced obesity in mice.

2011-06-01 | GSE26442 | GEO

Adipocyte-specific Steap4 deficiency reduced thermogenesis and energy expenditure in mice

Project description:Steap4, highly expressed in adipose tissue, is associated with metabolic homeostasis. Dysregulated adipose and mitochondrial metabolism contribute to obesity, highlighting the need to understand their interplay. Whether and how Steap4 influences mitochondrial function, adipocytes, and energy expenditure remains unclear. Adipocyte-specific Steap4-deficient mice exhibited increased fat mass and severe insulin resistance in our high-fat diet model. Mass spectrometry identified two classes of Steap4 interactomes: mitochondrial proteins and proteins involved in splicing. RNA-seq analysis of white adipose tissue demonstrated that Steap4 deficiency altered RNA splicing patterns with enriched mitochondrial functions. Indeed, Steap4 deficiency impaired respiratory chain complex activity, causing mitochondrial dysfunction in white adipose tissue. Consistently, brown adipocyte-specific Steap4 deficiency impaired mitochondrial function, increased brown fat whitening, reduced energy expenditure, and exacerbated insulin resistance in a high-fat model. Overall, our study highlights Steap4’s critical role in modulating adipocyte mitochondrial function, thereby controlling thermogenesis, energy expenditure, and adiposity.

2025-02-03 | GSE247291 | GEO

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]

Project description:Analysis of brown adipose tissue from Yin Yang 1 (YY1) brown fat specific knockout mice fed a high fat diet for 3 months. YY1 deficiency in brown adipose tissue leads to strong thermogenic deficiency. The goal was to identify the genes controlled by YY1 responsible of brown fat defective function. Control mice YY1flox/flox versus YY1flox/flox; Ucp1Cre were fed a high fat diet for 3 months

2015-11-10 | E-GEOD-68429 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data