Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The affect of loss of Casz1 in C2C12 cells on super-enhancers

ABSTRACT: In the differereniated C2C12 cells, knockdown of Casz1 leads to a re-establishment of super-enhancers

ORGANISM(S): Mus musculus

PROVIDER: GSE126141 | GEO | 2019/12/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The affect of loss of Casz1 in C2C12 cells on super-enhancers

Project description:The affect of loss of Casz1 in C2C12 cells on super-enhancers

| PRJNA521145 | ENA

RNA-sequencing analysis to investigate genes regulated by CASZ1 in C2C12 cells

Project description:RNA-sequencing analysis to investigate genes regulated by CASZ1 in C2C12 cells

| PRJNA521142 | ENA

CASZ1 is essential for activation of epidermal terminal differentiation

Project description:CASZ1 is a novel and potent activator of terminal epidermal differentiation. CASZ1 knockdown inhibits transcription of the epidermal differentiation program. p63 and p300 are required to activate CASZ1 expression.

2024-02-26 | GSE241873 | GEO

TMT analysis of TBX20:CASZ1 mutant mice with dilated cardiomyopathy

Project description:Using an unbiased systems-based screen, we demonstrate the cardiac transcription factor TBX20 physically and genetically interacts with the essential transcription factor CASZ1. This interaction is required for survival as mice heterozygous for both Tbx20 and Casz1 die post-natally as a result of dilated cardiomyopathy (DCM).We have used quantitative proteomic approaches to define the molecular pathways mis-regulated in Tbx20 and Casz1 mice and thus, are associated with DCM. Using an unbiased systems-based screen, we demonstrate the cardiac transcription factor TBX20 physically and genetically interacts with the essential transcription factor CASZ1. This interaction is required for survival as mice heterozygous for both Tbx20 and Casz1 die post-natally as a result of dilated cardiomyopathy (DCM).We have used quantitative proteomic approaches to define the molecular pathways mis-regulated in Tbx20 and Casz1 mice and thus, are associated with DCM.

2022-05-27 | PXD005788 | Pride

RNA-sequencing analysis to investigate genes regulated by CASZ1 in C2C12 cells

Project description:In this study we identified genes regulated by CASZ1b in C2C12 cells

2019-12-26 | GSE126144 | GEO

Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

Project description:MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.

2019-12-26 | GSE126143 | GEO

Role of CASZ1 in keratinocyte differentiation [CUT&RUN]

Project description:Here we indentified CASZ1 as an essential regulator of the epidermal differentiation program.

2024-04-16 | GSE261527 | GEO

Role of CASZ1 in keratinocyte differentiation [RNA-seq]

Project description:Here we indentified CASZ1 as an essential regulator of the epidermal differentiation program.

2024-04-16 | GSE261518 | GEO

Regulation of retinal development by a Casz1 chromatin remodelling complex

Project description:Analysis of chromatin accessibility and histone marks on control or Casz1 conditional mutant retinal cells

2022-02-01 | GSE126838 | GEO

Transcriptional super-enhancers connected to cell identity and disease

Project description:Super-enhancers are large clusters of transcriptional enhancers that drive expression of genes that control and define cell identity. Improved understanding of the roles super-enhancers play in biology would be afforded by knowing the constellation of factors that constitute these domains and by identifying super-enhancers across the spectrum of human cell types. We describe here the population of transcription factors, cofactors, chromatin regulators and core transcription apparatus that occupy super-enhancers in embryonic stem cells (ESCs) and evidence that super-enhancers are highly transcribed. We then use epigenomic data to produce a catalogue of super-enhancers in a broad range of human cell types. These super-enhancer domains are associated with genes encoding master transcription factors and other components that play important roles in the biology of these cells. Interestingly, sequence variation associated with a broad spectrum of diseases is especially enriched in the super-enhancers of disease-relevant cell types. Furthermore, we find that cancer cells generate super-enhancers at oncogenes and other genes that play important roles in tumor pathogenesis. We discuss these insights and their implications for future study of human health and disease. ChIP-Seq for transcription factors in mouse embryonic stem cells and H3K27ac in Jurkat T-ALL cell line RNA-Seq for mouse embryonic stem cells

2013-10-23 | E-GEOD-51522 | biostudies-arrayexpress

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