Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Purinergic P2Y6 receptors function in brown adipose tissue

PROVIDER: PRJNA607327 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11105032.fastq.gz	Fastqsanger.gz
	SRR11105033.fastq.gz	Fastqsanger.gz
	SRR11105034.fastq.gz	Fastqsanger.gz
	SRR11105035.fastq.gz	Fastqsanger.gz
	SRR11105036.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Project description:Purinergic P2Y6 receptors function in white adipose tissue

| PRJNA607321 | ENA

Physiological functions of the RORs in brown adipose tissue

Project description:To determine the physiological targets of the RORs in brown adipose tissue. Keywords: Nuclear receptors, RORs, adipose

2008-12-18 | GSE9969 | 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.

2015-11-10 | GSE68429 | GEO

Sympathetic inputs regulate adaptive thermogenesis in brown adipose tissue through cAMP-Salt inducible kinase axis

Project description:Various physiological stimuli, such as cold environment, diet, and hormones, trigger brown adipose tissue (BAT) to produce heat through sympathetic nervous system (SNS)- and -adrenergic receptors (ARs). The AR stimulation increases intracellular cAMP levels through heterotrimeric G proteins and adenylate cyclases, but the processes by which cAMP modulates brown adipocyte function are not fully understood. Here we described that specific ablation of cAMP production in brown adipocytes led to reduced lipolysis, mitochondrial biogenesis, uncoupling protein 1 (Ucp1) expression, and consequently defective adaptive thermogenesis. Elevated cAMP signaling by sympathetic activation inhibited Salt-inducible kinase 2 (Sik2) through protein kinase A (PKA)-mediated phosphorylation in brown adipose tissue. Inhibition of SIKs enhanced Ucp1 expression in differentiated brown adipocytes and Sik2 knockout mice exhibited enhanced adaptive thermogenesis at thermoneutrality in an Ucp1-dependent manner. Taken together, our data indicate that suppressing Sik2 by PKA-mediated phosphorylation is a requisite for SNS-induced Ucp1 expression and adaptive thermogenesis in BAT, and targeting Sik2 may present a novel therapeutic strategy to ramp up BAT thermogenic activity in humans.

2018-07-12 | PXD009262 | Pride

Brown Adipose Tissue

Project description:Brown Adipose Tissue

| PRJNA1046054 | ENA

Loss of mouse P2Y6 nucleotide receptor is associated with physiological macrocardia and amplified pathological cardiac hypertrophy

Project description:The study of the mechanisms leading to cardiac hypertrophy is essential to better understand cardiac development and regeneration. Pathological conditions such as ischemia or pressure overload can induce a release of extracellular nucleotides within the heart. We recently investigated the potential role of nucleotide P2Y receptors in cardiac development. We showed that adult P2Y4-null mice displayed microcardia resulting from defective cardiac angiogenesis. Here we show that loss of another P2Y subtype called P2Y6, a UDP receptor, was associated with a macrocardia phenotype and amplified pathological cardiac hypertrophy. Cardiomyocyte proliferation and size were increased in vivo in hearts of P2Y6-null neonates, resulting in enhanced post-natal heart growth. We then observed that loss of P2Y6 receptor enhanced pathological cardiac hypertrophy induced after isoproterenol injection. We identified an inhibitory effect of UDP on in vitro isoproterenol-induced cardiomyocyte hyperplasia and hypertrophy. The present study identifies mouse P2Y6 receptor as a regulator of cardiac development and cardiomyocyte function. P2Y6 receptor could constitute a therapeutic target to regulate cardiac hypertrophy.

2016-12-19 | GSE76215 | GEO

The shared PPARα/γ target genes regulate brown adipocyte thermogenic function (ChIP-Seq)

Project description:We report the application of sequencing technology for high-throughput profiling of PPARα/γ in mammalian cells. By obtaining over 3 billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse brown adipose tissue. We find that PPARα binds to a subset of PPARγ sites, suggesting a potential redundancy in which PPARα function may not be necessary in brown adipose tissue.While PPARα may not itself be necessary for BAT function, shared targets regulation by PPARα and PPARγ may nonetheless reveal relevant biology in this tissue.This study provides a framework for the application of comprehensive chromatin profiling towards characterization of PPARα/γ regulation in mouse brown adipose tissue.

2020-01-30 | GSE144488 | GEO

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

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

Prdm16 Knockout Brown Adipose Tissue

Project description:Gene expression profile from brown adipose tissues of Prdm16 knockout and wile type mice. Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development.

2014-04-09 | GSE55080 | GEO

iBAT histone modification ChIP seq of wild type C57BL/6N mice exposed to cold and high fat diet.

Project description:Cold and nutrient activated brown adipose tissue (BAT) is capable of increasing systemic energy expenditure via uncoupled respiration and secretion of endocrine factors thereby protecting mice against diet-induced obesity and improving insulin response and glucose tolerance in men. Long non-coding RNAs (lncRNAs) have recently been identified as fine tuning regulators of cellular function. While certain lncRNAs have been functionally characterised in adipose tissue, their overall contribution in the activation of BAT remains elusive. We identified lncRNAs correlating to inter- scapular brown adipose tissue (iBAT) function in high fat diet (HFD) and cold stressed mice. We focused on Gm15551 which has an adipose tissue specific expression profile, is highly upregulated during adipogenesis and downregulated by β-adrenergic activation in mature adipocytes. Albeit we performed comprehensive transcriptional and adipocyte physiology profiling in vitro and in vivo, we could not detect an effect of gain or loss of function of Gm15551.

2022-05-12 | GSE200651 | GEO

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