Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE234825 | GEO | 2023/10/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [ncRNA-seq]

Project description:The list of circular RNAs (circRNAs) involved in tumor metabolic reprogramming is rapidly increasing, but whether circRNAs have a role in linking epigenetic modification with lipid metabolism remains elusive. Here, we demonstrate that the circRNA circEPB41(2), which expression is driven by HNRNPA1 in response to glucose deprivation, is important for de novo lipogenesis. Moreover, we uncovered a genome-wide decrease in specific histone acetylation after circEPB41(2) depletion. These changes are associated with altered gene expression and observed cellular phenotypes, suggesting their functional significance. Mechanistically, we showed that circEPB41(2) regulates histone acetylation in part by modulating the stability and polyadenylation of SIRT6 through binding and maintaining the demethylase activity of FTO. Accordingly, circEPB41(2) silencing inhibited cellular lipid accumulation, suppressed cell proliferation, and inhibited cancer xenograft growth. Thus, circEPB41(2) may consider a target for cancer treatment.

2024-07-25 | GSE272595 | GEO

Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [RNA-seq]

2023-10-11 | GSE234823 | GEO

Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [H3K9ac ChIP-seq]

2023-10-11 | GSE234822 | GEO

Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications

Project description:Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications

| PRJNA983290 | ENA

Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [ncRNA-seq]

Project description:Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [ncRNA-seq]

| PRJNA1137400 | ENA

Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [RNA-seq]

Project description:Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [RNA-seq]

| PRJNA983299 | ENA

Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [H3K9ac ChIP-seq]

Project description:Energy stress-induced circEPB41(2) regulates lipogenesis through histone modifications [H3K9ac ChIP-seq]

| PRJNA983297 | ENA

The histone methyltransferase G9a regulates tolerance to oxidative stress-induced energy consumption.

Project description:Stress responses are crucial processes that require activation of genetic programs that protect from the stressor. Stress responses are also energy consuming and can thus be deleterious to the organism. The mechanisms coordinating energy consumption during stress response in multicellular organisms are not well understood. Here, we show that loss of the epigenetic regulator G9a in Drosophila causes a shift in the transcriptional and metabolic responses to oxidative stress (OS) that leads to decreased survival time upon feeding the xenobiotic paraquat. During OS exposure, G9a mutants show overactivation of stress response genes, rapid depletion of glycogen, and inability to access lipid energy stores. The OS survival deficiency of G9a mutants can be rescued by a high-sugar diet. Control flies also show improved OS survival when fed a high-sugar diet, suggesting that energy availability is generally a limiting factor for OS tolerance. Directly limiting access to glycogen stores by knocking down glycogen phosphorylase recapitulates the OS-induced survival defects of G9a mutants. We propose that G9a mutants are sensitive to stress because they experience a net reduction in available energy due to (1) rapid glycogen use, (2) an inability to access lipid energy stores, and (3) an overinduced transcriptional response to stress that further exacerbates energy demands. This suggests that G9a acts as a critical regulatory hub between the transcriptional and metabolic responses to OS. Our findings, together with recent studies that established a role for G9a in hypoxia resistance in cancer cell lines, suggest that G9a is of wide importance in controlling the cellular and organismal response to multiple types of stress.

| S-EPMC6413895 | biostudies-literature

The histone acetyltransferase PCAF regulates p21 transcription through stress-induced acetylation of histone H3.

Project description:The activity of p53 as a tumor suppressor primarily depends on its ability to transactivate specific target genes in response to genotoxic and other potentially mutagenic stresses. Several histone acetyl transferases (HATs), including p300, CBP, PCAF and GCN5 have been implicated in the activation of p53-dependent transcription of the cyclin-dependent kinase (cdk) inhibitor p21 as well as other target genes. Here we show that PCAF, but not CBP or p300, is a critical regulator of p53-dependent p21 expression in response to multiple p53-activating stresses. PCAF was required for the transcriptional activation of p21 in response to exogenous p53 in p53-null cells, nutlin-3, DNA damaging agents and p14(ARF) expression, suggesting a broad requirement for PCAF in p53 signaling to p21 after stress. Importantly, cells lacking PCAF failed to undergo cell cycle arrest in response to nutlin-3 treatment or p14(ARF) expression, consistent with a physiologically important role for PCAF in this p53 function. Surprisingly, the role for PCAF in induction of p21 was independent of p53 lysine 320 acetylation, a previously suggested target of PCAF-mediated acetylation. Though p21 promoter occupancy by p53 was not altered by PCAF knockdown, activation of p21 transcription required an intact PCAF HAT domain, and induction of chromatin marks acetyl-H3K9 and acetyl-H3K14 at the p21 promoter by p53 was dependent upon physiologic levels of PCAF. Together, our experiments indicate that PCAF is required for stress-responsive histone 3 acetylation at the p21 promoter, p53-directed transcription of p21 and the resultant growth arrest.

| S-EPMC3404877 | biostudies-other

Tribbles-1 regulates hepatic lipogenesis through post-transcriptional regulation of C/EBPα

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-07-14 | GSE70848 | GEO