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

PROVIDER: PRJNA601452 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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 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

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 ATAC-seq.

2020-03-09 | GSE144428 | GEO

Comparison of retinal gene expression among Chx10-cre;Tsc f/f, Chx10-cre;Tsc+/+ and 24-month-old C57BL/6 mice

Project description:Comparison of retinal gene expression among Chx10-cre;Tsc f/f, Chx10-cre;Tsc+/+ and 24-month-old C57BL/6 mice

| PRJNA736942 | ENA

Comparison of retinal gene expression among Chx10-cre;Tsc f/f, Chx10-cre;Tsc+/+ and 24-month-old C57BL/6 mice

Project description:Retina aging is the main cause of vision decline in elderly population and it is also an important risk factor for the development of degenerative and angiogenic retinal diseases. Therefore it is important to explore the mechanisms which drive retina aging. In this study, we found that retina from old-aged mice had increased mTORC1 activity. Whole transcriptome microarray expression profiling of the retina tissue among among Wild Type Control, Chx10-specific Tsc1 knockout and natural aging mice showed that the most significantly enriched Gene Ontology terms were substantially in common in knockout and aging mice compared to Control mice. we further demonstrated that the activation of mTORC1 in Chx10-expressing cells led to accelerated retina aging and degeneration, with significant functional decline measured by electroretinogram, ganglion cell senescence, microglial cell activation and the accumulation of oxidative stress and inflammatory responses. Inhibition of microglial cells by minocycline partially prevented photoreceptor cell loss and restored the electroretinogram responses. The results demonstrated that mTORC1 activation accelerated retina aging, suggested that microglial cell contributed significantly to overall retinal degeneration.

2021-06-12 | GSE177039 | GEO

Transcription profiling of mouse Rb1 deficient Apc1638N cecal tumors vs duodenal tumors

Project description:To examine the role of Rb1 in gastrointestinal (GI) tumors we generated mice with an Apc1638N allele, Rbtm2brn floxed alleles, and a villlin-cre transgene (RBVCA). These mice had reduced median survival due to an increase in tumor incidence and multiplicity in the cecum and the proximal colon; they differed from murine intestinal tumors of the Apc1638N type which normally arise solely in the small intestine. We have examined by micro-array analysis three cecal tumors from these mice (probable adenomas), and compared them to three duodenal tumors (probable adenocarcinomas). Expression profiles of duodenal and cecal tumors relative to each other show unique gene subsets up and down regulated. The two tumor types were subsequently shown to differentially regulate distinct sets of genes over expressed in a majority of human colorectal carcinomas. Experiment Overall Design: We have compared 3 cecal tumors with 3 duodenal tumors from Rb1 deficient Apc1638N mice.

2008-11-13 | E-GEOD-13298 | biostudies-arrayexpress

Chx10 consolidates V2a interneuron identity through two distinct gene repression modes [RNA-Seq]

Project description:During development, two cell-types born from closely related progenitor pools often express the identical transcriptional regulators despite their completely distinct characteristics. This phenomenon highlights the necessity of the mechanism that operates to segregate the identities of the two cell-types throughout differentiation after initial fate commitment. To understand this mechanism, we investigated the fate specification of spinal V2a interneurons, which share important developmental genes with motor neurons (MNs). Here we demonstrate that the paired homeodomain factor Chx10 functions as a critical determinant for V2a fate and is required to consolidate V2a identity in postmitotic neurons. Chx10 actively promotes V2a fate, downstream of the LIM-homeodomain factor Lhx3, while concomitantly suppressing MN developmental program by preventing the MN-specific transcription complex from binding and activating MN genes. This dual activity enables Chx10 to effectively separate V2a and MN pathways. Together, our study uncovers a widely applicable gene regulatory principle for segregating related cell fates. RNA samples from Chx10-ESC-derived MNs were prepared for sequencing according to the Illumina protocol, and sequenced on the Illumina HiSeq 2000. We will then compare the transcriptome changes between -Dox (no Chx10) and +Dox (Chx10) in order to identify genes rregulated by Chx10.

2016-07-28 | E-GEOD-83873 | biostudies-arrayexpress

Expression data from murine fetal liver cells, combinations of RB1 family 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 | GSE67276 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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