Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Zfp352 over expression ATAC-seq result

ABSTRACT: Zfp352 over expression ATAC-seq result

PROVIDER: PRJNA922926 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23049206_1.fastq.gz	Fastqsanger.gz
	SRR23049206_2.fastq.gz	Fastqsanger.gz
	SRR23049207_1.fastq.gz	Fastqsanger.gz
	SRR23049207_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Zfp352 over expression ATAC-seq result

Project description:Our data delineated bifurcated binding and regulation of ZFP352 towards two distinct retrotransposons, MT2_Mm and SINE_B1/Alu,and whether ZFP352 can regulate mouse genome openness remains unknown,here we conduct ATAC-seq of Zfp352 over expression sample to detect ZFP352's role in regulating chromatin openness.

2023-06-01 | GSE222635 | GEO

Zfp352 over expression chip-seq result

Project description:Zfp352 over expression chip-seq result

| PRJNA834815 | ENA

Zfp352 and Zfp352+Dux over expression chip-seq result

Project description:Zfp352 and Zfp352+Dux over expression chip-seq result

| PRJNA922927 | ENA

Zfp352 and Zfp352+Dux over expression chip-seq result

Project description:Our data delineated bifurcated binding and regulation of ZFP352 towards two distinct retrotransposons, MT2_Mm and SINE_B1/Alu,further ChIP-seq experiments validated that over-expression of Dux displaced ZFP352 from SINE_B1/Alu and DUX-independent ZFP352 binding sites, but promoted ZFP352 binding onto MT2_Mm and DUX_ZFP352 co-bound sites

2023-06-01 | GSE222634 | GEO

Zfp352 over expression chip-seq result

Project description:Previous study has determined Dux regulates 2CLC trancriptome via binding and activating MERVL,but the mechanism about the change happned during the 2C-exit process are rarely determined.In this study,we try to illustrate how ZFP352 binds genome location to regulate its downstream trancriptome and 2C-exit process.And make some conclusion and hypothesis about ZFP352 co-binding and interact with other trancription factor:Dux,etc to regulate 2C-exit.

2023-06-01 | GSE202158 | GEO

Transcriptome analysis in mouse ES cells deficient for Zfp352 or both Zfp352/Zfp353

Project description:Mouse ES cell population contains a minor sub-population expressing the genes that are specifically expressed in 2-cell stage embryos. This sub-population, consists of the 2-cell-gene labelled cells (2CLCs), is generated by the transient activation of the 2-cell specific genes initiated by the master regulator Dux. However, the mechanism regulating the transient expression remains largely unclear. Here we reported a novel function of Zfp352, one of the 2-cell specific genes, in the regulation of the 2CLC sub-population. Zfp352 encodes zinc-finger transcription factor belonging to the Klf family. Zfp352 is transiently activated by Dux after the activation of Zscan4c and expresses in a subset of 2CLC subpopulation. Interestingly, in the reporter assay, the transcriptional activation of Zscan4c by Dux is strongly repressed by the co-expression of Zfp352. However, knockout of Zfp352 resulted in the repression of a subset of the 2-cell specific genes. These data suggest the dual roles of Zfp352 in the regulation of the transient activation of the 2-cell specific genes.

2023-09-18 | GSE242542 | GEO

Knocking down Zfp352 delayed mouse embryo development

Project description:To explore the function of ZFP352 during mouse early embryonic development, siRNA targeting Zfp352 was injected into the zygotes and the effect of Zfp352 depletion on development was followed.

2023-06-01 | GSE224628 | GEO

Selective binding of retrotransposons by ZFP352 facilitates the timely dissolution of totipotency network

Project description:Acquisition of new stem cell fates relies on the dissolution of the prior regulatory network sustaining the existing cell fates. Currently, extensive insights have been revealed for the totipotency regulatory network around the zygotic genome activation (ZGA) period. However, how the dissolution of the totipotency network is triggered to ensure the timely embryonic development following ZGA is largely unknown. In this study, we identified the unexpected role of a highly expressed 2C embryo specific transcription factor, ZFP352, in facilitating the dissolution of the totipotency network. We found that ZFP352 has bifurcated binding and regulation towards two different retrotransposon sub-families. ZFP352 coordinates with DUX to bind and regulate the 2C specific MT2_Mm sub-family. On the other hand, without DUX, ZFP352 switched affinity to bind extensively onto SINE_B1/Alu sub-family. This leads to the activation of later developmental programs like ubiquitination pathways, to facilitate the dissolution of the 2C state. Correspondingly, depleting ZFP352 in mouse embryos impaired the 2C to morula transition process. Thus, through differential regulation of MT2_Mm and SINE_B1/Alu, ZFP352 can trigger spontaneous dissolution of the totipotency network. Our study highlights the importance of different retrotransposons sub-families in facilitating the timely and programmed cell fates transition during early embryogenesis.

2023-06-01 | GSE222636 | GEO

Transcriptome analysis in mouse ES cells deficient for Zfp352 or both Zfp352/Zfp353

Project description:Transcriptome analysis in mouse ES cells deficient for Zfp352 or both Zfp352/Zfp353

| PRJNA1013900 | ENA

Project description:SAGA and ATAC are two related transcriptional coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development but the precise role of the two complexes in RNA polymerase II transcription in mammals is less understood. To determine whether SAGA and ATAC have redundant or specific functions dependent on their HAT activities, we compared the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC subunits are required for complex assembly, mouse ESC growth and self-renewal. Additionally, ATAC, but not SAGA subunits are required for ESC viability by regulating the transcription of translation-related genes. Surprisingly, depletion of specific or shared HAT module subunits caused a global decrease in histone H3K9 acetylation, but did not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for viability and self-renewal of mouse ESCs by regulating transcription through different pathways, in a HAT-independent manner.

2021-08-11 | PXD027026 | 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