Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Rb family triple knock out liver progenitor cells

ABSTRACT: This serie was performed on liver progenitor isolated based on their expression of the Sca1 surface marker. It contains two independent samples from Rb family deficient liver and three independent samples from control liver, all isolated 2 weeks after Tamoxifen-induced Rb family ablation. Hematopoietic (CD45, Ter119) and endothelial (CD31) markers were used as negative selection markers to exclude blood or endothelial cells from the isolated fraction.

ORGANISM(S): Mus musculus

PROVIDER: GSE63793 | GEO | 2015/11/15

SECONDARY ACCESSION(S): PRJNA269076

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from WT, E2f8 KO, Rb KO and Rb;E2f8 DKO spleen Ter19+CD71high sorted cells

Project description:To understand molecular mechanisms underlying the synergy of Rb loss and E2F8 loss, we used gene expression profiling to assess molecular changes in Mx1-Cre-mediated knockout (KO) mice using RNA isolated from sorted Ter119+CD71high Erythroblasts. The top four upregulated and enriched pathways in the DKO mice included DNA replication, DNA damage response, DNA repair, and RNA processing. Interestingly, the majority of upregulated genes in the enriched sections of the four shared pathways contain E2f binding site(s) in their promoters, suggesting that Rb and E2F8 largely repress those genes through the E2f binding sites. Collectively, our data suggest that Rb and E2F8 co-regulate E2F-responsive genes. Spleen Ter119+CD71high cells were sorted from WT, E2f8 KO, Rb KO and E2f8;Rb DKO mice

2014-05-30 | E-GEOD-52157 | biostudies-arrayexpress

Expression data from WT, E2f8 KO, Rb KO and Rb;E2f8 DKO spleen Ter19+CD71high sorted cells

2014-05-30 | GSE52157 | GEO

TRANSCRIPTIONAL ACTIVATION BY E2F4 INDEPENDENT OF THE RB FAMILY

Project description:E2F transcription factors are central regulators of cell cycle progression and cell fate decisions in mammalian cells. E2F4 is a transcriptional repressor implicated in cell cycle arrest and whose repressive activity depends on its interaction with members of the RB family. E2F4 often represents the predominant E2F activity in cells. Here we show that E2F4 is important for the proliferation and the survival of mouse embryonic stem cells. In these cells, E2F4 acts in part as a transcriptional activator that promotes the expression of cell cycle genes. Importantly, this role for E2F4 is completely independent of the RB family. Accordingly, an unbiased analysis of the E2F4 interactome shows that E2F4 functionally interacts with chromatin regulators associated with gene activation in RB family-mutant cells. Taken together, our findings uncover a non-canonical role for E2F4 that reveal novel insights into the biology of rapidly dividing cell types.

2019-04-26 | PXD008796 | Pride

Expression data from Rb family (Rb, p130 and p107) deficient Hematopoietic stem Cells

Project description:Loss of Rb family in HSCs results in a severe phenotype, such as enhanced proliferation and increase in stem cell number. In addition, HSCs were higly mobilized but failed to transplant. Rb family deficient mice rapidly exhibit a myeloproliferative disease with eosinophilic characteristics. Meanwhile, the lymphoid compartment was severely decreased, due to high apoptotic activity in this lineage. Keywords: unpaired WT versus Rb family deficient KLS

2008-04-25 | GSE11253 | GEO

Expression data from early and macroscopic HCC lesions isolated from the Rb family Triple Knock Out model (ATAC-Seq)

Project description:we report the chromatin conformation profile of various liver progenitor subpopulations upon inactivation of the Rb family of proteins.

2024-05-05 | GSE173948 | GEO

Expression data from early and macroscopic HCC lesions isolated from the Rb family Triple Knock Out model (Bulk RNA-Seq)

Project description:we report the expression profiles of various liver progenitor subpopulations upon inactivation of the Rb family of genes

2024-05-05 | GSE173949 | GEO

Transcription profiling of mouse Rb family triple knock-out (TKO) embryonic stem cells as they differentiate in vivo

Project description:The retinoblastoma cell cycle regulator pRb and the two related proteins p107 and p130 are thought to suppress cancer development both by inhibiting the G1/S transition of the cell cycle in response to growth-arrest signals and by promoting cellular differentiation. Here, we investigated the phenotype of Rb family triple knock-out (TKO) embryonic stem cells as they differentiate in vivo and in culture. Confirming the central role of the Rb gene family in cell cycle progression, TKO mouse embryos did not survive past mid-gestation and differentiating TKO cells displayed increased proliferation and cell death. However, patterning and cell fate determination were largely unaffected in these TKO embryos. Furthermore, a number of TKO cells, including in the neural lineage, were able to exit the cell cycle in G1 and terminally differentiate. This ability of Rb family TKO cells to undergo cell cycle arrest was associated with the repression of target genes for the E2F6 transcription factor, uncovering a pRb-independent control of the G1/S transition of the cell cycle. These results show that the Rb gene family is required for proper embryonic development but is not absolutely essential to induce G1 arrest and differentiation in certain lineages. Experiment Overall Design: Genome-wide gene expression was analyzed for wild-type and TKO ESC and EB cells. Three biological replicates were isolated for wild-type ESCs, TKO ESCs, and wild-type EBs, while five biological replicates were isolated for TKO EBs.

2009-09-12 | E-GEOD-13408 | biostudies-arrayexpress

Expression data from wildtype and Rb-/- fetal liver at e12.5

Project description:Rb null embryos exhibit defective fetal liver erythropoiesis. We used microarrays to compare Wt and Rb null fetal livers and to analyse gene expression differences which accompany and may underlie Rb null fetal liver degeneration, erythroid failure, and erythropoietic island dissolution. We used microarrays to compare Wt and Rb null fetal livers and analyse gene expression changes which accompany and may underlie fetal liver. Keywords: retinoblastoma, fetal liver, erythroblast, macrophage, cell death

2007-06-05 | GSE6787 | GEO

Amycolatopsis mediterranei RB strain:RB

Project description:Amycolatopsis mediterranei RB strain:RB Genome sequencing

| PRJNA172643 | ENA

E2F4 regulates transcriptional activation in mouse embryonic stem cells independently of the RB family

Project description:E2F transcription factors are central regulators of cell division and cell fate decisions. E2F4 often represents the predominant E2F activity in cells. E2F4 is a transcriptional repressor implicated in cell cycle arrest and whose repressive activity depends on its interaction with members of the RB family. Here we show that E2F4 is important for the proliferation and the survival of mouse embryonic stem cells. In these cells, E2F4 acts in part as a transcriptional activator that promotes the expression of cell cycle genes. This role for E2F4 is independent of the RB family. Accordingly, E2F4 functionally interacts with chromatin regulators associated with gene activation and we observed decreased histone acetylation at the promoters of cell cycle genes and E2F targets upon loss of E2F4 in RB family-mutant cells. Taken together, our findings uncover a non-canonical role for E2F4 that provide insights into the biology of rapidly dividing cells.

2019-04-25 | GSE109684 | 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