Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C [ChIP-seq]

ABSTRACT: We describe a methyl histone writer-eraser double-mutant animal that corrects phenotypes of single-mutants KMT2A and KDM5C.

ORGANISM(S): Mus musculus

PROVIDER: GSE127817 | GEO | 2020/06/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C [RNA-seq]

Project description:We describe a methyl histone writer-eraser double-mutant animal that corrects phenotypes of single-mutants KMT2A and KDM5C.

2020-06-16 | GSE127722 | GEO

Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C

Project description:Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C

| PRJNA525445 | ENA

Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C

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

2020-06-16 | GSE127818 | GEO

Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C [RNA-seq]

Project description:Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C [RNA-seq]

| PRJNA525106 | ENA

Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C [ChIP-seq]

Project description:Amelioration of Brain Histone Methylopathies by Balancing a Writer-Eraser Duo KMT2A-KDM5C [ChIP-seq]

| PRJNA525450 | ENA

NO001: Kdm5c controls promoter and enhancer activities

Project description:The functional organization of eukaryotic genomes correlates with specific patterns of histone methylations. Regulatory regions in genomes like enhancers and promoters differ in their extent of methylation of histone H3 at lysine-4 (H3K4), but it is largely unknown how the different methylation states are specified and controlled. Here, we show that the Kdm5c/Jarid1c/SMCX member of the Kdm5 family of H3K4 demethylases can be recruited to both enhancer and promoter elements in embryonic stem cells and neuronal progenitor cells via gene-specific transcription factors. Knockdown of Kdm5c deregulates transcription via local increases in H3K4me3. Our data show that restricting H3K4me3 modification at core promoters dampens transcription, but Kdm5c is required at enhancers for their full activity. Remarkably, an impaired enhancer function activates the intrinsic promoter activity of Kdm5c-bound distal elements. Our results demonstrate that the Kdm5c demethylase plays a crucial and dynamic role in the functional discrimination between enhancers and core promoters. RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells.

2013-04-05 | E-GEOD-38862 | biostudies-arrayexpress

The Kdm5c histone demethylase controls enhancer and promoter function.

Project description:Here, we show that the Kdm5c/Smcx member of the Jarid1 family of H3K4 demethylases is recruited to both enhancer and core promoter elements in ES and neuronal progenitor cells (NPC). Knockdown of Kdm5c deregulates transcription via a local increase in H3K4me3. While at core promoters the function of Kdm5c is to restrict transcription, loss of Kdm5c impairs enhancer function. Remarkably, an impaired enhancer function activates promoter activity from Kdm5c-bound intergenic regions. Our results demonstrate that the Kdm5c demethylase plays a crucial role in the functional identity and discrimination of enhancers and core promoters. We speculate that this is related to recruitment of H3K4me3 binders like the TFIID and NURF complexes6-8. Providing functional identity to genomic regions through balancing enzymes that deposit and remove histone modifications may prove to be a general epigenetic mechanism for the functional indexing of eukaryotic genomes. Examination of the KDM5C binding sites in mouse embryonic stem cells and in neuronal progenitor cells. Effect of KDM5C knock down on H3K4me3 and H3K4me1 levels and gene expression.

2013-04-01 | E-GEOD-34975 | biostudies-arrayexpress

NO001: Kdm5c controls promoter and enhancer activities

Project description:RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells

2013-04-05 | E-MTAB-1177 | biostudies-arrayexpress

Methylation Landscape: Targeting Writer or Eraser to Discover Anti-Cancer Drug.

Project description:Cancer is a major global health challenge for our health system, despite the important pharmacological and therapeutic discoveries we have seen since past 5 decades. The increasing prevalence and mortality of cancer may be closely related to smoking, exposure to environmental pollution, dietary and genetic factors. Despite significant promising discoveries and developments such as cell and biotechnological therapies a new breakthrough in the medical field is needed to develop specific and effective drugs for cancer treatment. On the development of cell therapies, anti-tumor vaccines, and new biotechnological drugs that have already shown promising effects in preclinical studies. With the continuous enrichment and development of chromatin immunoprecipitation sequencing (ChIP-seq) and its derivative technologies, epigenetic modification has gradually become a research hotspot. As key ingredients of epigenetic modification, Writers, Readers, Erasers have been gradually unveiled. Cancer has been associated with epigenetic modification especially methylation and therefore different epigenetic drugs have been developed and some of those are already undergoing clinical phase I or phase II trials, and it is believed that these drugs will certainly assist the treatment in the near future. With respect to this, an overview of anti-tumor drugs targeting modified enzymes and de-modified enzymes will be performed in order to contribute to future research.

| S-EPMC8209422 | biostudies-literature

Project description:BackgroundProtein post-translational modifications (PTMs) change protein properties. Each PTM type is associated with domain families that apply the modification (writers), remove the modification (erasers) and bind to the modified sites (readers) together called toolkit domains. The evolutionary origin and diversification remains largely understudied, except for tyrosine phosphorylation. Protein palmitoylation entails the addition of a palmitoyl fatty acid to a cysteine residue. This PTM functions as a membrane anchor and is involved in a range of cellular processes. One writer family and two erasers families are known for protein palmitoylation.ResultsIn this work we unravel the evolutionary history of these writer and eraser families. We constructed a high-quality profile hidden Markov model (HMM) of each family, searched for protein family members in fully sequenced genomes and subsequently constructed phylogenetic distributions of the families. We constructed Maximum Likelihood phylogenetic trees and using gene tree rearrangement and tree reconciliation inferred their evolutionary histories in terms of duplication and loss events. We identified lineages where the families expanded or contracted and found that the evolutionary histories of the families are correlated. The results show that the erasers were invented first, before the origin of the eukaryotes. The writers first arose in the eukaryotic ancestor. The writers and erasers show co-expansions in several eukaryotic ancestral lineages. These expansions often seem to be followed by contractions in some or all of the lineages further in evolution.ConclusionsA general pattern of correlated evolution appears between writer and eraser domains. These co-evolution patterns could be used in new methods for interaction prediction based on phylogenies.

| S-EPMC5359973 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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