Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analyses of hMADS cells depleted for hormone-sensitive lipase

ABSTRACT: Hormone-sensitive lipase HSL is a major metabolic enzyme of adipocyte as the rate limiting enzyme of lipolysis. Recently, a non enzymatic role of HSL as been described in the regulation of the Carbohydrate Responive Element Binding Protein (ChREBP), controlling adipocyte insulin sensitivity. We aimed at further explore new roles of HSL in the control of adipocyte metabolism through gene expression modulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE186544 | GEO | 2025/10/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptional regulation of adipocyte lipolysis by IRF2BP2 [ChIP-seq]

Project description:Adipocyte lipolysis controls systemic energy levels and metabolic homeostasis. Lipolysis is regulated by post-translational modifications of key lipolytic enzymes. However, less is known about the transcriptional mechanisms that regulate lipolysis. Here, we identify the transcriptional factor interferon regulatory factor-2 binding protein 2 (IRF2BP2) as a repressor of adipocyte lipolysis. Deletion of IRF2BP2 in primary human adipocytes increases lipolysis without affecting glucose uptake, whereas IRF2BP2 overexpression decreases lipolysis. RNA-seq and ChIP-seq analyses reveal that IRF2BP2 directly represses several lipolysis-related genes, including LIPE (HSL, hormone sensitive lipase), which encodes the rate-limiting enzyme in lipolysis. Adipocyte-selective deletion of Irf2bp2 in mice increases Lipe expression and free fatty acid levels, resulting in elevated adipose tissue inflammation and glucose intolerance. Altogether, these findings demonstrate that IRF2BP2 restrains adipocyte lipolysis and opens new avenues to target lipolysis for the treatment of metabolic disease.

2024-11-14 | GSE281495 | GEO

Transcriptional regulation of adipocyte lipolysis by IRF2BP2 [CUT&RUN]

2024-11-14 | GSE281494 | GEO

Transcriptional regulation of adipocyte lipolysis by IRF2BP2 [RNA-seq]

2024-11-14 | GSE281493 | GEO

Off-target effects of the lysosomal acid lipase inhibitors Lalistat-1 and Lalistat-2 on neutral lipid hydrolases

Project description:Lysosomal acid lipase (LAL) is the key enzyme of lysosomal lipid hydrolysis, which degrades cholesteryl esters (CE), triacylglycerols (TG), diacylglycerols (DG), and retinyl esters. The role of LAL in various cellular processes has mostly been studied in LAL-deficient (Lal-/-) mice, which share phenotypical characteristics with humans suffering from LAL deficiency. In vitro, the cell-specific functions of LAL have been commonly investigated by using the LAL inhibitors Lalistat-1 (L1) and Lalistat-2 (L2). Here, we show that pharmacological LAL inhibition but not genetic loss of LAL impairs isoproterenol-stimulated lipolysis and neutral TG hydrolase (TGH) and CE hydrolase (CEH) activities in mature adipocytes, indicating that L1 and L2 inhibit other lipid hydrolases apart from LAL. Since adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) are the major enzymes that degrade cytosolic TG and CE, respectively, at neutral pH, we hypothesized that L1 and L2 also inhibit ATGL and/or HSL through off-target effects. In fact, both inhibitors drastically reduced neutral CEH activity in cells overexpressing mouse and human HSL and neutral TGH activity in cells overexpressing mouse and human ATGL, albeit to a lesser extent. By performing serine hydrolase-specific activity-based labeling in combination with quantitative proteomics, we confirmed that L2 inhibits HSL and other lipid hydrolases, whereas L1 treatment results in less pronounced inhibition of neutral lipid hydrolases. These results demonstrate that commonly used concentrations of L2 (and L1) are not suitable for investigating the role of LAL-specific lipolysis in lysosomal function, signaling pathways, and autophagy.

2022-05-13 | PXD030672 | Pride

Transcriptomic analyses of hMADS cells depleted for hormone-sensitive lipase

Project description:Transcriptomic analyses of hMADS cells depleted for hormone-sensitive lipase

| PRJNA774345 | ENA

Lipolysis regulates major transcriptional programs in brown adipocytes [Lipase Inh. Exp]

Project description:β-Adrenergic signaling is a core regulator of brown adipocyte function stimulating both lipolysis and transcription of thermogenic genes, thereby expanding the capacity for oxidative metabolism. Here we have used pharmacological inhibitors and a novel direct activator of lipolysis to acutely modulate the activity of lipases, thereby enabling us to uncover lipolysis-dependent signaling pathways downstream of β-adrenergic signaling in brown adipocytes. We show that induction of lipolysis leads to acute induction of several gene programs and is required for transcriptional regulation by β-adrenergic signals. Using machine-learning algorithms to infer causal transcription factors, we show that PPARs are key mediators of lipolysis-induced activation of genes involved in lipid metabolism and thermogenesis. Importantly, lipolysis also activates the unfolded protein response and regulates the core circadian transcriptional machinery independently of PPARs. Our results demonstrate that lipolysis generates important metabolic signals that exert profound pleiotropic effects on brown adipocyte transcription and function.

2022-06-03 | GSE205134 | GEO

Transcription profiling of mouse liver samples comparing hormone sensitive lipase (HSL) knockout mice vs. wildtype

Project description:HSL is a key enzyme in in the mobilization of fatty acids from the triglyceride stores of white adipose tissue. In addition, it is expressed in mice liver. In the present microarray study, changes in the transcript profile of murine liver samples due to global HSL knockout were investigated. Experiment Overall Design: Genetic modification to analyze the impact of a general knockout of the HSL gene on liver metabolism. Experiment Overall Design: HSL knockout (ko) mice versus wildtype (wt) mice. Mice fed a normal diet (ND) versus mice fed a high fat diet (FD) for 6 months. Equal amounts of liver samples from six mice were pooled and total RNA was extracted, except for HSL-null mice on FD were only 4 livers were pooled.

2009-01-14 | E-GEOD-10067 | biostudies-arrayexpress

Metabolomics Workbench ST000662 - GNPS - Lipidomics of hormone-sensitive lipase variants

Project description:The samples are frozen biopsies of whilte subcutaneous adipose tissues (50 mg). Samples were collected from 4 hormone-sensitive lipase (HSL) WT patients (adipose insulin sensitive), 3 HSL heterozygote patients and 1 HSL KO patient.

2018-08-02 | MSV000082691 | GNPS

Gene expression data from murine liver samples comparing hormone sensitive lipase (HSL) knockout mice vs. wildtype mice

2009-01-03 | GSE10067 | GEO

Transcriptomic analysis of lipase TLL during the lipid expression process of Aspergillus niger at different time points.

Project description:Aspergillus Niger CICC2629 was used as the host strain to express Thermomyces lanuginosus lipase. The enzyme activity and enzymatic properties of the lipase were measured, and the expression ability of exogenous protein in the host strain was investigated using transcriptomics.

2025-08-01 | GSE302033 | 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