Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

ABSTRACT: We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Tumors from Rb1/p107 DKO and Rb1/p107/Hells TKO mice were analyzed for gene expression using RNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE143732 | GEO | 2020/03/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Retinae from Rb1/p107 DKO and Rb1/p107/Hells TKO mice at postnatal day 21 were analyzed for gene expression using RNA-seq.

2020-03-09 | GSE144427 | GEO

Chromatin accessibility analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

2020-03-09 | GSE144428 | GEO

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

Project description:Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

| PRJNA601452 | ENA

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

Project description:Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

| PRJNA603600 | ENA

Chromatin accessibility analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

Project description:Chromatin accessibility analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

| PRJNA603599 | ENA

Expression data from wild-type or Rb mutant MEFs

Project description:The retinoblastoma family regulates numerous genes in multiple biochemical processes including cell cycle, apoptosis, and cellular metabolic. We used multiple genetically modified cell lines in order to better understand the contributing role of each pocket protein to gene expression. Microarray analysis was performed on wild-type, Rb1 knock-out, triple knock-out (TKO: Rb1, p107, p130), or TKO-RasG12D mouse embryonic fibroblasts

2016-05-01 | GSE76542 | GEO

Expression data from murine fetal liver cells in culture, time course, combinations of RB1 and p107 knockouts

Project description:Retinoblastoma-1 (RB1), and the RB1-related proteins p107 and p130, reside at a central node in the cell cycle regulatory network. RB1 is required for normal erythroid development in vitro, but is largely dispensable for erythropoiesis in vivo. The modest phenotype caused by RB1 deficiency in mice raises questions about redundancy within the RB1 family, and the role of RB1 in erythroid differentiation. Here we show that RB1 is the major pocket protein that regulates terminal erythroid differentiation. Erythroid cells lacking all pocket proteins exhibit the same cell cycle defects as those deficient for RB1 alone. Further, we show that RB1 broadly represses gene expression in erythroid cells, coincident with the transition from precursor to terminally differentiated cell. RB1-repressed genes are well expressed but downregulated at the final stage of erythroid development. By merging differential and time-dependent changes in expression, we define a group of approximately 800 RB1-repressed genes. As anticipated, these genes are enriched for terms such as cell cycle and DNA metabolic process, but also for terms such as mRNA processing, chromosome organization, and ubiquitin-mediated protein catabolic pro-cess. Our results suggest that RB1-mediated repression of genes involved in noncanonical processes has a central role in terminal erythroid differentiation.

2015-10-01 | GSE67278 | GEO

Expression data from murine fetal liver cells, combinations of RB1 family knockouts

2015-10-01 | GSE67276 | GEO

The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

Project description:The activating E2F-transcription factors are best known for their dependence on the Retinoblastoma protein and their role in cellular proliferation. E2F3 is uniquely amplified in specific human tumours where its expression is inversely correlated with the survival of patients. Here, E2F3 interaction partners were identified by mass spectrometric analysis. We show that the SNF2-like HELLS interacts with E2F3 in vivo and cooperates with its oncogenic functions. Depletion of HELLS severely perturbs the induction of E2F-target genes, hinders cell cycle re-entry and growth. Using chromatin immmunoprecipitation coupled to sequencing we identified genome-wide targets of HELLS and E2F3. Our analysis revealed that HELLS binds near promoters of active genes, including the trithorax-related MLL1, and co-regulates E2F3-dependent genes. Our analysis is the first to link HELLS with E2F-controlled processes that are critical to establish a proliferative tumour circuitry. Strikingly, just as E2F3, HELLS is overexpressed in human tumours including prostate cancer, indicating that either factor may contribute to the malignant progression of tumours. Our work reveals that HELLS is important for E2F3 in tumour cell proliferation.

2011-12-19 | GSE33791 | GEO

The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

2011-12-19 | E-GEOD-33791 | biostudies-arrayexpress