Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94816 | GEO | 2018/10/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Next Generation Sequencing Facilitates Quantitative Analysis of KMT2D Knockdown/Control PC-3 Cell Line Transcriptomes

Project description:KMT2D is a histone methyltransferase for catalyzing the monomethylation of H3K4. Previous studies have indentified that H3K4me1 is prominent on active enhancers and participates in gene expression regulation. To further examine the transcriptional changes in response to KMT2D depletion, we performed RNA-seq with KMT2D knockdown and control PC-3 cells by BGISEQ-500

2018-10-23 | GSE94807 | GEO

DNA hypermethylation encroachment at CpG island borders in cancer is predisposed by H3K4 monomethylation [WGBS_Mm]

Project description:The crosstalk between H3K4 monomethylation and DNA methylation has been receiving little attention to date. We investigated a mouse model harboring a loss-of-function mutation of lysine methyltransferase 2D (KMT2D), which catalyzes the monomethylation of lysine 4 on histone H3. We performed H3K4me1 ChIP-seq in spleen B cells with the wild type (WT) KMT2D as well as heterozygous (HET) and homozygous (HOM) chr15: 98,835,228 A>T KMT2D mutation. Alongside, using WGBS, we performed genome-wide DNA methylation profiling in spleen B cells with the WT KMT2D as well as HET and HOM chr15: 98,835,228 A>T KMT2D mutation.

2019-01-23 | GSE104781 | GEO

DNA hypermethylation encroachment at CpG island borders in cancer is predisposed by H3K4 monomethylation [ChIP-Seq]

2019-01-23 | GSE104533 | GEO

Investigating the regulatory role of KMT2D in neurodeveolopment using organoid and single cell techniques

Project description:Enhancer-mediated gene activation of lineage-specifiers, together with extrinsic niche factors, determines cell fate. Mutations in KMT2D, the H3K4me1-catalyzing enhancer-activator, result in ~70% of the KABUKI syndrome, a neurodevelopmental disorder. Yet the impacted cell-of-origin and the bona fide targets of KMT2D in human neurodevelopment are missing. Here we applied cerebral organoid and single-cell technologies to delineate human-specific distal regulatory elements across heterogeneous cell types.

2024-09-06 | GSE183627 | GEO

KMT2D regulates Fanconi anemia pathway genes through regulating promoters/enhances upon glucose deprivation (CHIPseq)

Project description:Histone H3 lysine (H3K4) methyltransferase KMT2D is a key regulator of gene expression, mainly through promoting H3K4 methylation and activating enhancers, and plays critical roles in development, differentiation, metabolism, and tumor suppression. Here, our study showed that KMT2D was recruited to the enhancer regions of several Fanconi anemia (FA) pathway genes, such as ATR, FANCM, REV3L, and TOP3A, in response to glucose deprivation. Notably, KMT2D loss led to significant impairment of promoter/enhancer signals, as evidenced by decreased H3K4me1, H3K4me3, and H3K27ac signals, on several FA pathway genes. Our ChIP-Seq results demonstrated that the inactivation of promoters/enhancers due to KMT2D loss is a key contributor to the downregulation of FA pathway genes in glucose-deprived KMT2D-deficient HNSCC.

2024-07-01 | GSE234640 | 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

Analysis of KMT2D Knockdown/Control PC-3 Cell Line

Project description:Analysis of KMT2D Knockdown/Control PC-3 Cell Line

| PRJNA374508 | ENA

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

Gene regulation profiling by KMT2D under different glucose conditions in HNSCC (RNAseq)

2024-07-01 | GSE237454 | GEO

Identification of H3 Lysine 4 Monomethylation Associated Proteins at Mammalian Enhancers

Project description:Enhancers act to regulate cell type specific gene expression by facilitating the transcription of target genes. In mammalian cells active or primed enhancers are commonly marked by monomethylation of Histone H3 at lysine 4 (H3K4me1) in a cell-type specific manner. Whether and how this histone modification regulates enhancer-dependent transcription programs in mammals has been unclear. In the present study, we conducted SILAC Mass-spec experiments with mono-nucleosomes and identified multiple H3K4me1 associated proteins, including proteins involved in chromatin remodeling. We demonstrate that H3K4me1 augments the association of the chromatin remodeling complex BAF to enhancers in vivo. Furthermore we show that in vitro, H3K4me1 nucleosomes are more efficiently remodeled by the BAF complex. Crystal structures of a BAF component BAF45c further reveal that monomethylation, but not trimethylation, is accommodated in this protein’s H3K4 binding site. Our results suggest that H3K4me1 plays an active role at enhancers by facilitating the binding of the BAF complex and possibly other chromatin regulators.

2018-10-23 | PXD007942 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data