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KDM4B epigenetically protects against obesity and metabolic dysfunction

ABSTRACT: KDM4B epigenetically protects against obesity and metabolic dysfunction

PROVIDER: PRJNA397224 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5889221.fastq.gz	Fastqsanger.gz
	SRR5889222.fastq.gz	Fastqsanger.gz
	SRR5889223.fastq.gz	Fastqsanger.gz
	SRR5889224.fastq.gz	Fastqsanger.gz

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KDM4B epigenetically protects against obesity and metabolic dysfunction [gene expression]

Project description:KDM4B (lysine demethylase 4B) in adipose tissues plays a critical role in energy balance, oxidation, lipolysis and thermogenesis. Loss of KDM4B in mice resulted in obesity associated with reduced energy expenditure and impaired adaptive thermogenesis. Mechanistically, we determined that KDM4B directly controls the expression of multiple metabolic genes.

2019-05-22 | GSE102289 | GEO

KDM4B epigenetically protects against obesity and metabolic dysfunction [ChIP-seq]

Project description:Preadiocyte of Kdm4b KO mice was infected with control or Flag-KDM4B retrovirus and were differentiated to adipocyte. The well-differentiated adipocytes were harvested for ChIP-Seq with Flag antibody.

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KDM4B epigenetically protects against obesity and metabolic dysfunction

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Project description:KDM4B epigenetically protects against obesity and metabolic dysfunction [ChIP-seq]

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Mus musculus

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KDM4B protects against obesity and metabolic dysfunction.

Project description:Although significant progress has been made in understanding epigenetic regulation of in vitro adipogenesis, the physiological functions of epigenetic regulators in metabolism and their roles in obesity remain largely elusive. Here, we report that KDM4B (lysine demethylase 4B) in adipose tissues plays a critical role in energy balance, oxidation, lipolysis, and thermogenesis. Loss of KDM4B in mice resulted in obesity associated with reduced energy expenditure and impaired adaptive thermogenesis. Obesity in KDM4B-deficient mice was accompanied by hyperlipidemia, insulin resistance, and pathological changes in the liver and pancreas. Adipocyte-specific deletion of Kdm4b revealed that the adipose tissues were the main sites for KDM4B antiobesity effects. KDM4B directly controlled the expression of multiple metabolic genes, including Ppargc1a and Ppara Collectively, our studies identify KDM4B as an essential epigenetic factor for the regulation of metabolic health and maintaining normal body weight in mice. KDM4B may provide a therapeutic target for treatment of obesity.

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INPP4B protects from metabolic disease and obesity associated prostate neoplasia.

Project description:A high fat diet and obesity have been linked to the development of metabolic dysfunction and the promotion of multiple cancers in mice and men. The causative cellular signals are multifactorial and not completely understood. Previous studies have shown that metabolic dysfunction leads to activation of the AKT and PKC pathways. Both signaling pathways are inhibited by the dual specificity phosphatase, INPP4B, which dephosphorylates PI(3,4)P2, an activator of AKT, and PI(4,5)P2, an activator of the PLC/PKC pathway. We established that INPP4B signaling protects mice from metabolic dysfunction. Inpp4b-/- male mice had accelerated activation of SREBF1 in liver which, along with the high fat diet, caused increased expression and activity of PPARG and other lipogenic pathways leading non-alcoholic fatty liver disease (NAFLD), type II diabetes, expansion and inflammation of WAT, and systemic and localized prostate inflammation that drives the development of high-grade prostatic intraepithelial neoplasia (PIN).

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Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity

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ChIP-seq of Danio rerio wild type and kdm4b mutant embryos to investigate kdm4b signaling

Project description:chromatin immunoprecipitation sequencing (ChIP-seq) was performed to identify the targeted genes of kdm4b

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Expression analysis of blastocysts in Kdm4b-PEs

Project description:To identify the genes that are controled by H3K9me3 modification in PEs, we conducted transcriptome analysis using Egfp-, Kdm4b-PEs, and IVF embryos at blastocyst stages. Kdm4b or Egfp mRNA injected oocytes were parthenogenetically activated. IVF embryos were generated according to standard protcol. All embryos were cultured in KSOM medium for 120 hours after activation or sperm insemination. Five blastocysts per one biological replicate were pooled and analyzed.

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