Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The lipid droplet protein DHRS3 is a regulator of melanoma cell state

ABSTRACT: The lipid droplet protein DHRS3 is a regulator of melanoma cell state

PROVIDER: PRJNA1090238 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28402082_1.fastq.gz	Fastqsanger.gz
	SRR28402082_2.fastq.gz	Fastqsanger.gz
	SRR28402083_1.fastq.gz	Fastqsanger.gz
	SRR28402083_2.fastq.gz	Fastqsanger.gz
	SRR28402084_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

The lipid droplet protein DHRS3 is a regulator of melanoma cell state

Project description:Lipid droplets are fat storage organelles composed of a protein envelope and a lipid rich core. Dynamic regulation of this protein envelope underlies differential lipid droplet formation and function in diverse cell types. In melanoma, the ability to form lipid droplets has been linked to tumor progression and metastasis, but it is not known whether lipid droplet proteins play a role in these phenotypes. To address this, we performed proteomic analysis of the lipid droplet envelope in melanoma. We found that proteins expressed in the lipid droplet were differentially enriched in distinct melanoma states, ranging from melanocytic to neural crest like. DHRS3, which is involved in the conversion of all-trans-retinal to all-trans-retinol, is significantly upregulated in the MITFLO/neural crest-like melanoma cell state, and markedly reduced in the MITFHI/melanocytic state. Increased DHRS3 expression is sufficient to drive the MITFHI/melanocytic cells to a more undifferentiated and invasive state. These changes are due to retinoic acid mediated regulation of melanocytic genes through the retinoid X receptors (RXR). Our data demonstrate that melanoma cell state can be regulated by expression of lipid droplet proteins which affect downstream retinoid signaling.

2024-03-25 | GSE262095 | GEO

Lipid droplets are a metabolic vulnerability in melanoma

Project description:Melanoma exhibits numerous transcriptional cell states including neural crest-like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here, we use a zebrafish melanoma model to identify a transcriptional program linking the melanocytic cell state to a dependence on lipid droplets, the specialized organelle responsible for lipid storage. Single-cell RNA-sequencing of these tumors show a concordance between genes regulating pigmentation and those involved in lipid and oxidative metabolism. This state is conserved across human melanoma cell lines and patient tumors. This melanocytic state demonstrates increased fatty acid uptake, an increased number of lipid droplets, and dependence upon fatty acid oxidative metabolism. Genetic and pharmacologic suppression of lipid droplet production is sufficient to disrupt cell cycle progression and slow melanoma growth in vivo. Because the melanocytic cell state is linked to poor outcomes in patients, these data indicate a metabolic vulnerability in melanoma that depends on the lipid droplet organelle.

2023-03-26 | GSE201378 | GEO

RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of aged mice

Project description:Sequencing data related to the manuscript entitled, "Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain".

2019-10-30 | GSE139542 | GEO

RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of Progranulin KO mice

Project description:Sequencing data related to the manuscript entitled, "Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain".

2019-11-07 | GSE140009 | GEO

RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of LPS-treated young mice

Project description:Sequencing data related to the manuscript entitled, "Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain".

2019-11-06 | GSE139946 | GEO

Microglial REV-ERBα regulates inflammation and lipid droplet formation to drive tauopathy

Project description:Alzheimer’s disease is associated with disrupted circadian rhythms and clock gene expression. REV-ERBα (Nr1d1) is a circadian transcriptional repressor involved in the regulation of lipid metabolism and macrophage function. While global REV-ERBα deletion increases microglial activation and mitigates amyloid plaque formation, the cell-autonomous effects of microglial REV-ERBα on tau pathology are unexplored. Here, we show that microglial REV-ERBα deletion enhances inflammatory signaling, disrupts lipid metabolic processes, and causes lipid droplet (LD) accumulation specifically in male microglia. Inflammation and LD accumulation combine to inhibit microglial tau phagocytosis, which can be partially rescued by blockage of lipid droplet formation. Microglial REV-ERBα deletion exacerbates tau aggregation and neuroinflammation in P301S and AAV-P301L tauopathy models in male, but not female mice. These data demonstrate the importance of microglial lipid droplets in tau accumulation and reveal REV-ERBα as a therapeutically accessible, sex-dependent regulator of microglial inflammatory signaling, lipid metabolism, and tauopathy.

2023-07-12 | GSE236875 | GEO

CLSTN3B promotes lipid droplet maturation and lipid storage in adipocytes

Project description:LUM1_969842: Brown adipocyte lipid droplet proteomics (Figure 4d): 126, 127N, 127C, 128N: WT 128C, 129N, 129C, 130N: KO (clstn3b-/-) LUM1_997681: White adipocyte lipid droplet proteomics (Figure 4e): 126, 127C, 127N, 128C, 128N: WT 129C, 129N, 130C, 130N, 131N: KO (clstn3b-/-)

| MSV000095763 | MassIVE

RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of aged mice

Project description:RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of aged mice

| PRJNA580234 | ENA

Microglial REV-ERBα regulates inflammation and lipid droplet formation to drive tauopathy

Project description:Alzheimer’s disease is associated with disrupted circadian rhythms and clock gene expression. REV-ERBα (Nr1d1) is a circadian transcriptional repressor involved in the regulation of lipid metabolism and macrophage function. While global REV-ERBα deletion increases microglial activation and mitigates amyloid plaque formation, the cell-autonomous effects of microglial REV-ERBα deletion in healthy brain and in tauopathy are unexplored. Here, we show that microglial REV-ERBα deficient enhances inflammatory signaling, disrupts lipid metabolism, and causes lipid droplet (LD) accumulation specifically in male microglia. Inflammation and LD accumulation combine to inhibit microglial tau phagocytosis, which can be partially rescued by blockage of lipid droplet formation. Microglial REV-ERBα deletion exacerbates tau aggregation and neuroinflammation in P301S and AAV-P301L tauopathy models in male, but not female mice. These data demonstrate the importance of microglial lipid droplets in tau accumulation and reveal REV-ERBα as a therapeutically accessible, sex-dependent regulator of microglial inflammatory signaling, lipid metabolism, and tauopathy.

2023-08-09 | PXD043877 | Pride

Lipid droplet membrane proteins ubiquitylation

Project description:This project was aimed to identify lipid droplet (LD) membrane proteins that are ubiquitylated. We isolated LDs from the livers of control and alcohol-fed rats and extracted LD membrane proteins.

2023-02-27 | PXD038662 | Pride

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