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Setd2 reprograns lipid metabolism for the resolution of inflammation via H3K36me3 modification

ABSTRACT: Setd2 reprograns lipid metabolism for the resolution of inflammation via H3K36me3 modification

PROVIDER: PRJNA593576 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10587819_1.fastq.gz	Fastqsanger.gz
	SRR10587819_2.fastq.gz	Fastqsanger.gz
	SRR10587820_1.fastq.gz	Fastqsanger.gz
	SRR10587820_2.fastq.gz	Fastqsanger.gz
	SRR10587821_1.fastq.gz	Fastqsanger.gz

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Setd2 reprograns lipid metabolism for the resolution of inflammation via H3K36me3 modification

Project description:Purpose: The goal of this study is to identify differential Setd2-mediated H3K36me3 modificaion in the resolution phase of inflammation induced by LPS Methods: We profiled chip-seq with H3K36me3 antibody in bone marrow-derived macrophages stimulated with LPS for 0h, 4h, 16h. Results: We find different H3K36me3 enrichment peaks under LPS stimulation at different time.

2024-11-13 | GSE141470 | GEO

Setd2 reprograns lipid metabolism for the resolution of inflammation

Project description:Setd2 reprograns lipid metabolism for the resolution of inflammation

| PRJNA593580 | ENA

Setd2-dependent H3K36me3 is required for Acrbp1 and protamine transcriptions and spermiogenesis in mice

Project description:Spermatogenesis is precisely cotrolled by complex gene expression programs and involves epigenetic reprogramming including histone modification and DNA methylation. Setd2 catalyzes the trimethylation of histone H3 Lys36 (H3K36me3) and plays key roles in embryonic stem cell differentiation and somatic cell development; however, its role in male germ cell development remains elusive. Here we demonstrate an essential role of Setd2 for spermiogenesis. We show that targeted knockout of Setd2 in germ cells causes aberrant spermiogenesis with acrosomal malformation before step 8 round spermatid stage, resulting in complete male infertile. Furthermore, we show a complete loss of H3K36me3 and a significant altered gene expression profile, including Acrbp1 and protamines, caused by Setd2 deficiency. Our findings reveal a previously underappreciated role of Setd2-dependent H3K36me3 for spermiogenesis and improved the understanding of epigenetic disorders underlying male infertility.

2018-04-28 | GSE108717 | GEO

Single-nucleotide resolution profiling of N6-methyladenosine in SETD2 knockdown HepG2 cells [m6A miCLIP-seq]

Project description:To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 knockdown and control HepG2 cells by miCLIP-seq, and found the depletion of H3K36me3 by SETD2 silencing globally reduced m6A in the human transcriptome.

2019-02-21 | GSE121942 | GEO

The SPOP-containing Complex Functions as an E3 Ligase for SETD2 to Regulate Gene-Specific H3K36me3-Coupled Alternative Splicing

Project description:H3K36me3 has been reported to associate with active gene expression, and SETD2 is the mainly methyltransferase for H3K36me3. We identified SPOP which is a CUL3 family protein as a E3 ligase for SETD2. Genome wide analysis by using ChIPSeq and RNASeq demonstrate that SPOP specificly eliminate H3K36me3 modification at target genes and resulted in alternative splicing of those target genes.

2016-11-10 | GSE75270 | GEO

Setd2 reprograns lipid metabolism for the resolution of inflammation II

Project description:Setd2 reprograns lipid metabolism for the resolution of inflammation II

| PRJNA593579 | ENA

Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in HepG2 cells: SETD2 knockdown and control cells

Project description:SETD2 is the specific methyltransferase of H3K36me3. To obtain SETD2-dependent landscape of H3K36me3 in human genome, we performed ChIP sequencing in SETD2 silenced and control HepG2 cells.

2019-02-21 | GSE110318 | GEO

H3K36me3 and H3K27me3 occupancy profiling by high throughput sequencing from setd2 wt and ko germinal center B cells and H3K27me3 occupancy profiling by high throughput sequencing from phf19 wt and ko germinal center B cells

Project description:Our study aims to understand the H3K36me3 and H3K27me3 genome-wide alterations by analysing CHIP-seq data between setd2 wt and ko germinal center B cells, characterize the function of H3K36me3 methyltransferase setd2 in H3K36me3 itself and H3K27me3, further we aim to H3K27me3 from phf19 ,which is H3K27me3 regulator, WT and KO group to investigate the mechanism of H3K36me3 dependent H3K27me3 modification introduced by setd2.

2024-09-14 | GSE184043 | GEO

Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [ChIP-Seq]

Project description:H3K36me3 catalyzed by histone methyltransferase SETD2 is one of the most conserved epigenetic marks from yeast to mammals. SETD2 is frequently mutated in multiple cancers and acts as a tumor suppressor. Here, utilizing a liver-specific deletion of Setd2 mice model, we found that Setd2 depletion is sufficient to trigger hepatocarcinoma (HCC) spontaneously. Meanwhile, in a DEN-induced HCC model, Setd2 depletion significantly promoted tumor number and size. The mechanistic study showed that Setd2 suppresses HCC not only through modulating DNA damage response, but also regulating lipid metabolism in liver. Setd2 deficiency down-regulated the expression of cholesterol efflux genes and caused lipid accumulation. ChIP-Seq analysis further revealed that Setd2 deletion induced AP-1 activation in liver, which was probably trigged by accumulated cholesterol. AP-1 is a well-known oncogene in HCC and inhibits p53 in Setd2-deficient cells. Taken together, we found the role of an important epigenetic gene in regulating cholesterol homeostasis and HCC, and revealed the underlying mechanisms.

2021-09-01 | GSE136743 | GEO

Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [RNA-Seq]

2021-09-01 | GSE136742 | GEO