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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE237363 | GEO | 2023/07/18

REPOSITORIES: GEO

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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

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

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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 [ChIP-seq]

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

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

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

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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]

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ChIP-sequencing of the H3K4me1/2 in crypts from mice intestinal epithelium with intestinal epithelium specific LSD1 knock out compared to wild type

Project description:To study the epigenetic regulation of intestinal epithelium we focus on the role of chromatin modulators. Lysine-specific histone demethylase 1a (KDM1A, LSD1) is one of the enzymes that can erase the H3K4me1/2 mark. To assess the role of LSD1 in intestinal epithelium we studied wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We found that KO mice completely lack Paneth cells, and have altered stem cell characteristics compared to WT littermates. To assess genome-wide H3K4me1/2 levels in WT and KO small intestines, we sorted small intestinal crypt cells, fixed them, isolated chromatin, and performed ChIP using an H3K4me1 and an H3K4me2 antibody as described in the protocols.

2020-11-16 | E-MTAB-7871 | biostudies-arrayexpress

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

TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment [ChIP-seq]

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