Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling of Setd5 mutant cortical neural progenitors

ABSTRACT: Setd5 inactivation in neural stem cells, zebrafish and mouse leads to a significant H3K36 hypo-methylation mostly detectable along the gene bodies. Consequently, this chromatin alteration perturbs RNA processing during elongation, compromising the transcriptional output. This gene dysregulation affects proliferative dynamics of NSCs and synaptic wiring in the neuronal derivatives, ultimately resulting in behavioral deficits in adult mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE103912 | GEO | 2019/09/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptional profiling of Setd5 mutant cortical tissue

Project description:Setd5 inactivation in neural stem cells, zebrafish and mouse leads to a significant H3K36 hypo-methylation mostly detectable along the gene bodies. Consequently, this chromatin alteration perturbs RNA processing during elongation, compromising the transcriptional output. This gene dysregulation affects proliferative dynamics of NSCs and synaptic wiring in the neuronal derivatives, ultimately resulting in behavioral deficits in adult mice.

2019-09-16 | GSE133090 | GEO

SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [ChIP-seq]

Project description:We assess the epigenetic function of Setd5 in mouse neural stem cells (NSCs), by profiling a panel of histone modifications and Setd5 binding in wild type and Setd5 heterozygous NSCs.

2019-07-10 | GSE104274 | GEO

SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [RNA-seq]

Project description:We assess the role of Setd5 on trancription elongation, by profiling nascent chromatin bound RNAs after DRB treatment an release, in wild type and Setd5 heterozygous mouse neural stem cells (NSCs).

2019-07-10 | GSE127004 | GEO

SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring

Project description:SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring

| PRJNA524158 | ENA

Transcriptional profiling of Setd5 heterozygous and knockout mouse embryonic stem cells

Project description:SET-domain containing proteins play a vital role in regulating gene expression during development through modifications in chromatin structure. To study molecular function of SET domain containing 5 (Setd5), we assessed global changes in the mouse embryonic stem cell transcriptome when Setd5 gene is knocked out.

2016-12-13 | E-MTAB-5189 | biostudies-arrayexpress

SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [ChIP-seq]

Project description:SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [ChIP-seq]

| PRJNA412216 | ENA

SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [RNA-seq]

Project description:SETD5 is a H3K36 methyltransferase which preserves transcriptional fidelity during brain development and neuronal wiring [RNA-seq]

| PRJNA524274 | ENA

Transcriptional profiling of Setd5 mutant cortical tissue

Project description:Transcriptional profiling of Setd5 mutant cortical tissue

| PRJNA549931 | ENA

Expression data from SETD5-expressing 3T3-L1 cells.

Project description:SETD5 target genes in 3T3-L1 cells were analyzed.

2021-10-25 | GSE183845 | GEO

SETD5 haploinsufficiency affects mitochondrial compartment in neural cells

Project description:Neurodevelopmental disorders (NDDs) are heterogeneous conditions due to alterations of a variety of molecular mechanisms and cell dysfunctions. Epigenetic basis of NDDs have been reported in an increasingly number of cases while mitochondrial dysfunctions are more common within NDD patients than in the general population. Here, we investigated experimental models of Setd5 haploinsufficiency, that leads to NDDs in humans due to chromatin defects, and uncovered that mitochondrial dysfunction participates in the pathogenesis. Mitochondrial impairment is facilitated by transcriptional aberrations that follow the decrease of SETD5 enzyme. Low levels of SETD5 resulted in fragmented mitochondria, less mitochondrial potential and ATP production both in neural precursors and neurons. Mitochondria were miss-localized in mutant neurons, with few organelles within neurites and synapses. Our study explores the epigenetics/mitochondria interplay as an important aspect of NDD pathophysiology and defines the impairments of mitochondrial functionality and dynamics as new therapeutic targets for disorders associated with loss of SETD5.

2023-01-05 | GSE222188 | GEO

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