Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MOF haploinsufficiency triggers diet-induced obesity resistance

ABSTRACT: MOF haploinsufficiency triggers diet-induced obesity resistance

PROVIDER: PRJNA658027 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12303181_1.fastq.gz	Fastqsanger.gz
	SRR12303181_2.fastq.gz	Fastqsanger.gz
	SRR12303182_1.fastq.gz	Fastqsanger.gz
	SRR12303182_2.fastq.gz	Fastqsanger.gz
	SRR12303183_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 44

Similar Datasets

MOF haploinsufficiency triggers diet-induced obesity resistance (ChIP-seq)

Project description:MOF haploinsufficiency triggers diet-induced obesity resistance (ChIP-seq)

| PRJNA658033 | ENA

MOF haploinsufficiency triggers diet-induced obesity resistance (RNA-seq)

Project description:MOF haploinsufficiency triggers diet-induced obesity resistance (RNA-seq)

| PRJNA648078 | ENA

MOF haploinsufficiency triggers diet-induced obesity resistance (RNA-seq)

Project description:Constant crosstalk between epigenetic regulators and metabolism homeostasis ensures that several tissues can respond and adapt to environmental cues. Decreased levels of the lysine acetyltransferase (KAT), MOF, was recently associated with cerebral development and syndromic intellectual disability. However, the consequences of having a chronic reduction of MOF levels are still unveiled. Here we characterized by FIA-MS/MS the metabolic profile of Mof heterozygous animals. We generated the profile of 8 different organs that have distinct metabolic demands. Overall, our analysis revealed that Mof heterozygous mice have impaired glucose homeostasis, fatty acids metabolism, and amino acid accumulation. When exposed ad libitum to high-fat diet those animals failed to gain fat mass, while the lean mass remains unalterable. At the molecular level, using the adipocyte model we found that Mof regulates the expression of PPARs and Slc2a4. In summary, we identified the first KAT that shows high-fat diet resistance and we propose that the chronic reduction of Mof impacts metabolic disorders.

2021-07-23 | GSE154967 | GEO

MOF haploinsufficiency triggers diet-induced obesity resistance (ChIP-seq)

Project description:Constant crosstalk between epigenetic regulators and metabolism homeostasis ensures that several tissues can respond and adapt to environmental cues. Decreased levels of the lysine acetyltransferase (KAT), MOF, was recently associated with cerebral development and syndromic intellectual disability. However, the consequences of having a chronic reduction of MOF levels are still unveiled. Here we characterized by FIA-MS/MS the metabolic profile of Mof heterozygous animals. We generated the profile of 7 different organs that have distinct metabolic demands. Overall our analysis reveled that Mof heterozygous mice have impaired glucose homeostasis, fatty acids metabolism, and amino acid accumulation. Furthermore, when exposed ad libitum to high-fat diet those animals failed to gain fat mass, while the lean mass remains unalterable. Accordingly, at the molecular level, using the adipocyte model we found that Mof regulates the expression of PPARs and Slc2a4. In summary, we identified the first KAT that shows high-fat diet resistance and we propose that the chronic reduction of Mof has a strong impact on metabolic disorders.

2021-07-23 | GSE156462 | GEO

Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity

Project description:Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity

| PRJEB11740 | ENA

MOF haploinsufficiency triggers diet-induced obesity resistance

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

2021-07-23 | GSE156463 | GEO

Promoter or enhancer activation by CRISPRa rescues haploinsufficiency caused obesity

Project description:Haploinsufficiency, having only one functional copy of a gene, leads to a wide-range of human diseases. Using obesity as a disease model, we tested whether haploinsufficiency can be rescued by CRISPR-mediated activation (CRISPRa) of the normal allele. Haploinsufficiency of either SIM1 or MC4R, results in severe obesity in humans and mice. In transgenic mice, CRISPRa targeting of the Sim1 promoter or its ~270kb distant hypothalamic enhancer, rescued the obesity phenotype in Sim1 heterozygous mice. Interestingly, despite using a ubiquitous promoter for CRISPRa, Sim1 was upregulated only in tissues where the promoter or enhancer are active, suggesting that cis-regulatory elements can determine CRISPRa tissue-specificity. To evaluate the potential therapeutic use of CRISPRa, we injected CRISPRa-rAAV into the hypothalamus, leading to reversal of the obesity phenotype in Sim1 and Mc4r heterozygous mice. Our results show that CRISPRa can be developed as a gene regulation therapy (GRT) to treat altered gene dosage diseases.

2018-12-17 | GSE112250 | GEO

KLF10 deficiency in CD4+ T cells triggers obesity and insulin resistance

Project description:KLF10 deficiency in CD4+ T cells triggers obesity and insulin resistance

| PRJNA588090 | ENA

Promoter or enhancer activation by CRISPRa rescues haploinsufficiency caused obesity

Project description:Promoter or enhancer activation by CRISPRa rescues haploinsufficiency caused obesity

| PRJNA445383 | ENA

Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity.

Project description:More than one-half billion people are obese, and despite progress in genetic research, much of the heritability of obesity remains enigmatic. Here, we identify a Trim28-dependent network capable of triggering obesity in a non-Mendelian, "on/off" manner. Trim28(+/D9) mutant mice exhibit a bi-modal body-weight distribution, with isogenic animals randomly emerging as either normal or obese and few intermediates. We find that the obese-"on" state is characterized by reduced expression of an imprinted gene network including Nnat, Peg3, Cdkn1c, and Plagl1 and that independent targeting of these alleles recapitulates the stochastic bi-stable disease phenotype. Adipose tissue transcriptome analyses in children indicate that humans too cluster into distinct sub-populations, stratifying according to Trim28 expression, transcriptome organization, and obesity-associated imprinted gene dysregulation. These data provide evidence of discrete polyphenism in mouse and man and thus carry important implications for complex trait genetics, evolution, and medicine.

| S-EPMC4735019 | biostudies-literature

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