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

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

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

Proteomic analysis of TAOK1 knockout in C2C12 myotubes

Project description:The establishment of C2C12 cell line with knockout of TAOK1 expression using CRISPR/Cas9 system. C2C12 cells with TAOK1 knockout were designated as C2C12-TAOK1-KO, while those transfected with an empty vector served as the control group (C2C12-Mock), non-transfected cells served as the blank group (C2C12-Blank). The C2C12-Blank, C2C12-Mock and C2C12-TAOK1-KO cells (10000 cells/mL) were seeded into 100 mm cell culture dishes and induced to differentiation into myotubes. Then, cells were obtained by trypsin digestion and centrifugation. Samples from three independent experiments were collected.

2024-10-23 | PXD057089 |

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