Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chip-Seq Raw data in LSD1 WT and KO mouse ES cells

ABSTRACT: LSD1, H3K4me1 and DNMT1 binding in LSD1 WT and KO mouse ES cells

PROVIDER: PRJEB78609 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR13448279_1.fastq.gz	Fastqsanger.gz
	ERR13448279_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

The catalytic-independent function of LSD1 modulates the epigenetic landscape of mouse embryonic stem cells

Project description:Lysine-specific histone demethylase 1 (LSD1), which demethylates mono- or di- methylated histone H3 on lysine 4 (H3K4me1/2), is essential for early embryogenesis and development. Here we show that LSD1 is dispensable for embryonic stem cell (ESC) self-renewal but is required for ESC growth and differentiation. Reexpression of a catalytically-dead LSD1 (LSD1MUT) recovers the proliferation capability of ESCs, yet the enzymatic activity of LSD1 is essential to ensure proper differentiation. Indeed, a gain of H3K4me1 in Lsd1 knockout (KO) ESCs does not lead to major changes in global gene expression programs related to stemness. However, ablation of LSD1 but not LSD1MUT results in decreased DNMT1 and UHRF1 proteins coupled to global hypomethylation. We show that both LSD1 and LSD1MUT control protein stability of UHRF1 and DNMT1 through interaction with the ubiquitin-specific peptidase 7 (USP7) and, consequently, inhibiting DNMT1 and UHRF1 ubiquitylation. Our studies elucidate for the first time a novel mechanism by which the scaffolding function of LSD1 controls DNA methylation in ESCs.

2024-08-03 | GSE273767 | GEO

Rybp ChIP-chip in mouse ES cells

Project description:Rybp binding in wild-type, Eed-KO, and Dnmt1-KO ES cells

2012-04-04 | GSE32289 | GEO

WGBS of WT and Smchd1-KO ES cells

Project description:WGBS of WT and Smchd1-KO ES cells

| PRJNA521987 | ENA

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

RNA-seq and expression profile of WT and ZFP57 KO ES cells

Project description:RNA-seq and expression profile of WT and ZFP57 KO ES cells

2011-11-07 | GSE31182 | GEO

ATAC-sequencing mice small 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 ATAC levels in WT and KO small intestines, we isolated intestinal epithelium tissue from wild type mice and LSD1 KO mice. This tissue was digested to single cells and performed ATAC seq as described in the protocols.

2021-03-23 | E-MTAB-8718 | biostudies-arrayexpress

Illumina microarray experiment on LSD1 deletion ES cell with Lsd1Lox/Δ3 and Lsd1Δ3/Δ3

Project description:Lysine specific demethylase 1 (LSD1), which demethylates mono- and di- methylated histone H3-Lys4 as part of a complex including CoREST and histone deacetylases (HDAC), is essential for embryonic development in the mouse beyond e6.5 days. Here, we demonstrate that LSD1 expression and therefore function, is restricted to the epiblast of the post- implantation embryo. Conditional deletion of LSD1 in mouse embryonic stem (ES) cells, in vitro counterpart of the epiblast, revealed a reduction in CoREST protein, a subsequent decrease in associated HDAC activity and a global increase in Histone H3 Lys56 acetylation. Despite this biochemical perturbation, LSD1 deleted ES cells proliferate normally and retain stem cell characteristics. Loss of LSD1 causes the aberrant expression of 588 genes, including a number of transcription factors with roles in tissue development such as brachyury, Hoxb7, Hoxd8 and RARγ. Brachyury, a key-regulator of mesodermal differentiation, is a direct target gene of LSD1 and is over-expressed in e6.5 day Lsd1 genetrap embryos. Thus, LSD1 is required for the appropriate expression of key developmental regulators, via the stabilization of the LSD1/CoREST/HDAC complex, during early embryonic development. RNA samples from Lsd1Lox/Δ3 and Lsd1Δ3/Δ3 cells were compared, three biological replicates were performed.

2010-12-06 | E-GEOD-21131 | biostudies-arrayexpress

RNA-seq of crypt cells from mouse small intestinal epithelium with an intestinal-epithelial specific deletion of LSD1 compared to wild type crypts

Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we isolated small intestinal crypts from wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We dissociated crypts into single cells, and FACS sorted Epcam+ cells, to avoid immune-cell contamination. RNA was directly isolated from these sorted cells, and this was used for RNA seq. As KO crypts are different from WT crypts (KO crypts lack Paneth cells), identifying genes specifically regulated by LSD1 helps us to identify how LSD1 regulates intestinal crypt biology. Specifically, because we were able to combine this with ChIP-seq of the same cells, to identify where H3K4me1 levels (target of the histone demethylase LSD1) were different in the genome.

2020-11-16 | E-MTAB-7862 | biostudies-arrayexpress

Transcriptome analysis of WT and ATRX KO Cast x 129 mouse ES cells

Project description:Analysis of gene expression in WT and ATRX KO Cast x 129 Mouse ES cells

2015-04-16 | GSE59269 | GEO

Illumina microarray experiment on LSD1 deletion ES cell with Lsd1Lox/Δ3 and Lsd1Δ3/Δ3

2010-12-06 | GSE21131 | GEO