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

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. Retinae from Rb1/p107 DKO and Rb1/p107/Hells TKO mice at postnatal day 21 were analyzed for gene expression using ATAC-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE144428 | GEO | 2020/03/09

REPOSITORIES: GEO

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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

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

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. Tumors from Rb1/p107 DKO and Rb1/p107/Hells TKO mice were analyzed for gene expression using RNA-seq.

2020-03-09 | GSE143732 | GEO

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

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

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 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

RNA-seq of human foreskin fibroblast cells lacking RB, p130, and p107 treated with doxorubicin.

Project description:We used human foreskin fibroblast cells with CRISPR-Cas9 mediated knockout of RB1 and p130 (RBL2) (sgP130, sgRB1+sg130), knocked down p107 using siRNA and measured gene expression changes after doxorubicin treatmnet (24 hr, 350 nM).

2019-10-10 | GSE135842 | GEO

p107 knockout vs. wild type neurospheres

Project description:The ganglionic eminence was dissected and neurospheres were cultured from the brain of E13.5 embroys. RNA was isolated from neurospheres cultured from p107-/- embryos and their wildtype littermates. P107 knockout mice have previously been shown to have an increased number of stem cells and enhanced stem cell self renewal. With the microarray experiment we are hoping to discover the genes involved in stem cell number and self renewal along with p107. Keywords: other

2005-12-09 | GSE3779 | GEO

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

2015-10-01 | GSE67276 | GEO

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