Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse AC61 cells were derived from a C-cell adenocarcinoma developed in Rb+/-N-ras-/- mouse transfected with pRb to identify genes that are regulated by pRb in AC61 cells

ABSTRACT: This experiment is to identify genes that are regulated by pRb in AC61 cells. AC61 cells were derived from a C-cell adenocarcinoma developed in an Rb+/-N-ras-/- mouse. Experiment Overall Design: AC61 cells were infected with retrovirus derived from pLXSB or pLSXB-Rb and selected with balsticidin for 36 hours. At 72 hour after infection, cells were quickly frozen.

ORGANISM(S): Mus musculus

SUBMITTER: Chiaki Takahashi

PROVIDER: E-GEOD-12637 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of mouse epidermis from Rb(F19/F19)K14cre;Rbl2-/- (pRb-;p130-) mutants to analyse functional redundancies between retinoblastoma family members

Project description:The epidermal-specific ablation of Rb gene leads to increased proliferation, aberrant differentiation, and the disengagement of these processes in vivo and in vitro. These differences in phenotype are more severe with the loss of p107, demonstrating the functional compensation between pRb and p107. As p107 and p130 also exert overlapping functions in epidermis, we have generated Rb(F19/F19)K14cre;Rbl2-/- (pRb-;p130-) mice to analyze possible functional redundancies between pRb and p130. The epidermal phenotype was very similar between pRb- and pRb-;p130- mice, suggesting that pRb and p130 activities are not redundant in epidermis. Importantly, we can correlate the proliferation differences with specific changes in gene expression between pRb-, pRb-;p107- and pRb-;p130- primary keratinocytes using microarray analysis, and explain the phenotypes in the context of altered E2F expression and functionality. Our findings support a model in which the distinct retinoblastoma family members, in conjunction with E2F members, play a central role in regulating epidermal homeostasis through specific or overlapping activities. Experiment Overall Design: Total RNA from pooled cells from each genotype were analyzed, per duplicate (pRb-/-;p107-/-, or pRb-/-;p130-/-) or triplicate (wild type, or pRb-/-), in mouse microarrays. Comparison was performed between the 4 different genotypes.

2008-06-16 | E-GEOD-9562 | biostudies-arrayexpress

RNAi profiling of human SAOS-2 cells, RBP2 knockdown or pRB overexpression

Project description:RBP2 is downstream of pRB pathway; We used gene expression profiling experiments to investigate if gene expression changes in cells with RBP2 knockdown significantly overlap with gene expression changes in cells overexpressing pRB, consistent with the data that knockdown of RBP2 phenocopies reintroduction of pRB in SAOS-2 (RB-/-) cells Experiment Overall Design: Knockdown of RBP2 by siRNA to RBP2 (RBP2siRNA) in SAOS-2 (RB-/-) cells in comparison to overexpression of pRB in the SOAS-2 (RB-/-) cells and scrambled version of the RBP2 siRNA (RBP2scsiRNA)

2008-10-25 | E-GEOD-9690 | biostudies-arrayexpress

AC61 Vector vs. pRb

Project description:This experiment is to identify genes that are regulated by pRb in AC61 cells. AC61 cells were derived from a C-cell adenocarcinoma developed in an Rb+/-N-ras-/- mouse.

2009-01-01 | GSE12637 | GEO

Transcription profiling of mouse placentas from wild-type and Rb -/- knock-out mice and embronic day 11.5 placentas from wild-type and Rb -/-;E2f4 -/- double knock-outs reveals E2F4 cooperates with pRB in the development of extra-embryonic, not embryonic, tissues

Project description:Homozygous mutation of the murine retinoblastoma tumor suppressor gene, Rb, results in embryonic lethality between E13.5 and E15.5 with defects in cellular proliferation, differentiation and apoptosis. Many of these defects are suppressed by mutation of an activating E2F, E2f1 or E2f3, indicating that they are key downstream targets of the retinoblastoma protein, pRB. In this study, we assess how E2F4 contributes to the developmental consequences of pRb-loss. In stark contrast to the activating E2Fs, the homozygous mutation of E2f4 shortened the lifespan of Rb-/- embryos. This resulted from an exacerbation of the placental defect of the Rb-/- mice indicating that E2F4 and pRB cooperate in the development of this tissue. Further analyses indicated that this defect reflects an increase in trophectoderm-like cells. Under conditions where the placenta was wild-type but the embryo mutant for E2f4 and pRb embryos survived to birth and exhibited all of the defects that were observed in the E2f4 and Rb single mutant embryos. Thus, while pRB and E2F4 cooperate in placental development, they play largely non-overlapping roles the development of many embryonic tissues. Experiment Overall Design: In one experiment, embryonic Day 13.5 placentas from wild-type and Rb -/- knock-out mice were compared. In the second experiment, embronic day 11.5 placentas from wild-type and Rb -/-;E2f4 -/- double knock-out mice were compared.

2009-06-24 | E-GEOD-13753 | biostudies-arrayexpress

SAOS-2 cells, RBP2 knockdown or pRB overexpression

Project description:RBP2 is downstream of pRB pathway We used gene expression profiling experiments to investigate if gene expression changes in cells with RBP2 knockdown significantly overlap with gene expression changes in cells overexpressing pRB, consistent with the data that knockdown of RBP2 phenocopies reintroduction of pRB in SAOS-2 (RB-/-) cells Keywords: epistatic experiment

2008-08-29 | GSE9690 | GEO

E2F4 cooperates with pRB in the development of extra-embryonic, not embryonic, tissues

2009-06-08 | GSE13753 | GEO

p107 acts as a tumor suppressor in pRb-deficient epidermis.

Project description:The specific deletion of Rb gene in epidermis leads to altered proliferation and differentiation, but not to the development of spontaneous tumors. Our previous data have demonstrated the existence of a functional compensation of Rb loss by Rbl1 (p107) in as the phenotypic differences with respect to controls are intensified. However, the possible evolution of this aggravated phenotype, in particular in relationship with tumorigenesis, has not been evaluated due to the premature death of the double deficient mice. We have now investigated whether p107 can also act as a tumor suppressor in pRb-deficient epidermis using different experimental approaches. We found spontaneous tumor development in doubly-deficient skin grafts. Moreover, Rb-deficient keratinocytes are susceptible to Ha-ras-induced transformation, and this susceptibility is enhanced by p107 loss. Further functional analyses, including microarray gene expression profiling, indicated that the loss of p107, in the absence of pRb, produces the reduction of p53-dependent pro-apoptotic signals. Overall, our data demonstrate that p107 behaves as a tumor suppressor in epidermis in the absence of pRb and suggest novel tumor-suppressive roles for p107 in the context of functional p53 and activated Ras Keywords: epidermis, tumorigenesis, pRb, p107, Ras, p53, apoptosis

2007-11-13 | GSE9567 | GEO

ATM mediates pRB function to control DNMT1 protein stability and DNA methylation

Project description:The retinoblastoma tumor suppressor gene (RB) product has been implicated in epigenetic control of gene expression owing to its ability to physically bind to many of chromatin modifiers. However, the biological and clinical significance of this activity was not well elucidated. To address this, we performed genetic and epigenetic analyses in an Rb-deficient mouse thyroid C cell tumor model. Here we report that the genetic interaction of Rb and ATM regulates DNMT1 protein stability, and hence controls the DNA methylation status in the promoter of at least Ink4a, Shc2, FoxO6 and Noggin genes. Further, we demonstrate that inactivation of pRB promotes the Tip60 (acetyltransferase)-dependent ATM activation, allows activated ATM to physically bind to DNMT1 forming a complex with Tip60 and UHRF1 (E3 ligase), and consequently accelerates DNMT1 ubiquitination driven by Tip60-dependent acetylation. Our results indicate that inactivation of pRB pathway in coordination with aberration in DNA damage response leads to abnormal DNA methylation pattern by affecting the stability of DNMT1. 163; Rb-/-;ATM-/- MEFs, D4; DNMT1 knockdown from 163 cells and analysed at day 4, WT8S; 163 cells reconstituted with ATM expression vector

2013-05-31 | E-GEOD-47501 | biostudies-arrayexpress

ATM mediates pRB function to control DNMT1 protein stability and DNA methylation

2013-05-31 | GSE47501 | GEO

Triple SILAC identified progesterone-independent and dependent PRA and PRB interacting partners in human breast cancer cells

Project description:Progesterone receptor (PR) isoforms, PRA and PRB, both progesterone-independent and dependent modulated the biology of breast cancer cells. The different phenotypes in breast cancer mediated by PRA and PRB could due to the differences of their structures, leading to the distinct protein interacting partners and downstream signaling events of each receptor. Here, we constructed Tet-inducible HA-tagged PRA or HA-tagged PRB in T47DC42 breast cancer cells. We performed affinity purification coupled with SILAC mass spectrometry technique to comprehensively study PRA and PRB interacting partners in both liganded and unliganded conditions. To validate our findings, we applied both forward and reverse SILAC to effectively minimize experimental errors. These datasets will be useful in investigating PRA- and PRB-specific molecular mechanisms and can potentially be used as a database for subsequent experiments to identify novel PRA and PRB interacting proteins that differentially mediated different biological functions in breast cancer cells.

2021-03-08 | PXD023920 | 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