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EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [Cut&Tag]

ABSTRACT: EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [Cut&Tag]

PROVIDER: PRJNA994830 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25277703_1.fastq.gz	Fastqsanger.gz
	SRR25277703_2.fastq.gz	Fastqsanger.gz
	SRR25277704_1.fastq.gz	Fastqsanger.gz
	SRR25277704_2.fastq.gz	Fastqsanger.gz
	SRR25277705_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [Cut&Tag]

Project description:CUT-Tag revealed a strong reduction of KMT2D, H3K4me1 and EBF2 signals at the transcription start site (TSS) and promoter regions of genes that were downregulated in KMT2D-depleted (KMT2D-KD) cells

2023-07-18 | GSE237365 | GEO

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [ChIP-seq]

Project description:ChIP-seq revealed a strong reduction of KMT2D, H3K4me1 and EBF2 signals at the transcription start site (TSS) and promoter regions of genes that were downregulated in KMT2D-depleted (KMT2D-KD) cells

2023-07-18 | GSE237364 | GEO

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [RNA-seq]

Project description:We sought to elucidate the roles of KMT2D- and EBF2-regulated H3K4me1 in gene expression through profiling the gene transcription in PDAC cells overexpressed with EBF2 (EBF2-OE) or activated by GSK-LSD1, a selective inhibitor of KDM1A/LSD1 which can increase H3K4me1 level via blocking the histone H3K4 demethylase activity of KDM1A/LSD1

2023-07-18 | GSE237363 | GEO

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN.

Project description:EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN.

| PRJNA994823 | ENA

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [RNA-seq]

Project description:EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [RNA-seq]

| PRJNA994828 | ENA

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [ChIP-seq]

Project description:EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [ChIP-seq]

| PRJNA994829 | ENA

EBF2 Links KMT2D-Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN.

Project description:Mono-methylation of histone H3 on Lys 4 (H3K4me1), which is catalyzed by histone-lysine N-methyltransferase 2D (KMT2D), serves as an important epigenetic regulator in transcriptional control. In this study, the authors identify early B-cell factor 2 (EBF2) as a binding protein of H3K4me1. Combining analyses of RNA-seq and ChIP-seq data, the authors further identify killin (KLLN) as a transcriptional target of KMT2D and EBF2 in pancreatic ductal adenocarcinoma (PDAC) cells. KMT2D-dependent H3K4me1 and EBF2 are predominantly over-lapped proximal to the transcription start site (TSS) of KLLN gene. Comprehensive functional assays show that KMT2D and EBF2 cooperatively inhibit PDAC cells proliferation, migration, and invasion through upregulating KLLN. Such inhibition on PDAC progression is also achieved through increasing H3K4me1 level by GSK-LSD1, a selective inhibitor of lysine-specific demethylase 1 (LSD1). Taken together, these findings reveal a new mechanism underlying PDAC progression and provide potential therapeutic targets for PDAC treatment.

| S-EPMC10787067 | biostudies-literature

EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN.

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

2023-07-18 | GSE237366 | GEO

H3K4me2 and gene expression profiling in control and KMT2D KD murine B220 cells

Project description:Define and compare H3K4me2 enrichment in murine B220 cells transduced with empty vector (ct) or KMT2D-shRNA. Compare gene expression by RNAseq in murine B220 cells transduced with empty vector (ct) or KMT2D-shRNA. Using H3K4me1/2 ChIPseq and RNAseq we profiled murine B220 purified cells from tumors transduced with EV (n=3) or KMT2D-shRNA (n=3).

2015-08-28 | E-GEOD-67291 | biostudies-arrayexpress

Genome-wide maps of chromatin state difference in KMT2D Knockdown/Control PC-3 Cells

Project description:KMT2D is a histone methyltransferase for catalyzing the monomethylation of H3K4. The H3K4me1 is prominent on active enhancers and participates in gene expression regulation. Loss of KMT2D in cancer has been approved to impact on a set of gene expression by the reduction of H3K4me1 level. To identify the direct target of KMT2D in prostate cancer, we performed H3K4me1 ChIP-seq with KMT2D knockdown and control PC-3 cells.

2018-10-23 | GSE94816 | GEO

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