Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of DNA methylation in stable gene repression

ABSTRACT: The experiment was designed to study the effects of the Dnmt1 gene knockout on gene expression, as well as to analyze the effects of TSA treatment on both WT (p53-/-) and knockout (p53-/-Dnmt1-/-) cells The effect of TSA treatment on knockout and WT cells was tested at two different time points (24 and 48 hs), as well as two weeks after removal of TSA Keywords: Effect of demetyhlation and/or reacetylation on gene expression

ORGANISM(S): Mus musculus

PROVIDER: GSE3534 | GEO | 2007/03/06

SECONDARY ACCESSION(S): PRJNA93589

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of mouse Dnmt1 knockouts and TSA treated p53-/- and p53-/-Dnmt1-/- cells to investigate the role of DNA methylation in stable gene repression

Project description:The experiment was designed to study the effects of the Dnmt1 gene knockout on gene expression, as well as to analyze the effects of TSA treatment on both WT (p53-/-) and knockout (p53-/-Dnmt1-/-) cells ; The effect of TSA treatment on knockout and WT cells was tested at two different time points (24 and 48 hs), as well as two weeks after removal of TSA Experiment Overall Design: Seven hybridizations were performed: 1. p53-/- untreated (control), 2. p53-/- +TSA harvested after 24hs of exposure to TSA, 3. p53-/- +TSA 48hs, 4. p53-/-Dnmt1-/- untreated, 5.p53-/-Dnmt1-/- +TSA 24hs 6.p53-/-Dnmt1-/- +TSA 48hs 7.p53-/-Dnmt1-/- two weeks after removal of TSA

2008-06-12 | E-GEOD-3534 | biostudies-arrayexpress

DNAJA1 KO on HUVECs with heat stress

Project description:HS-induced proteome changes in WT and DNAJA1-KO cells were quantified using label free-based quantitative proteomic analysis. Four groups:wild type HUVECs group, DNAJA1 knockout HUVECs group, WT HUVECs with heat stress group, DNAJA1 knockout HUVECs with heat stress group,were conducted label free-based quantitative proteomic analysis to detect the mechanism of DNAJA1's protective effects on heat stress.

2024-03-26 | PXD043512 | Pride

Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [S2]

Project description:Heat shock (HS) causes dramatic and rapid changes in transcription of thousands of genes in metazoans. We have used insitu Hi-C in Drosophila S2 and human K562 cells to determine the effects of HS upon chromatin conformation. Our study shows that topologically associated domains (TADs), compartments and distal regulatory interactions remain unchanged upon HS.

2019-06-07 | GSE130776 | GEO

Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [K562]

2019-06-07 | GSE130758 | GEO

Reprogramming of transcriptome after hormetic heat stress by the endoribonuclease ENDU 2 improves lifespan and stress resistance in C. elegans

Project description:Organisms' ability to respond to life-threatening environmental impacts is crucial for their survival. While acute stress responses to unfavorable factors are well known, the physiological consequences of transient stress experiences over time, as well as their underlying mechanisms, are not well understood. In this study, we investigated the long-term effects of a short heat shock (HS) exposure on the transcriptome of C. elegans. We found that the canonical HS response was followed by a profound transcriptional reprogramming affecting many genes involved in innate immunity response. This reprogramming relies on the endoribonuclease ENDU-2 but not the heat shock factor 1 (HSF-1). ENDU-2 in this context co-localizes with chromatin and interacts with RNA polymerase Pol II, enabling specific regulation of transcription in the post-HS period. Failure to activate this post-HS response does not impair animal survival under continuous HS insult but eliminates the beneficial effects of hormetic HS. In summary, our work discovers that the RNA-binding protein ENDU-2 mediates the hormetic long-term effects of transient HS to determine aging and longevity.

2023-06-29 | PXD041872 | Pride

Conditional knockdown of DNA methyltransferase-1 (Dnmt1) reveals a key role of retinal pigment epithelium integrity in photoreceptor outer segment morphogenesis

Project description:To explore the epigenetic contribution to retinal development, we generated conditional knockout alleles of DNA methytransferase-1 (Dnmt1) mediated by Rx-Cre in mice. The results demonstrate a unique function of DNMT1-mediated DNA methylation in controlling RPE apicobasal polarity and neural retina differentiation. Retinal samples were harvested from both Dnmt1 mutant and wt animals at embryonic day 16.5 and postnatal days 0.5, 6.5, and 10.5 for microarray analysis. Each experiment was performed with biological quadruplicates. One microgram of total RNA was used for cDNA systhesis in target molecule production.

2013-01-31 | E-GEOD-43951 | biostudies-arrayexpress

Effect of wtp53-reactivating drug RITA on HCT116 cells

Project description:Since its discovery as a tumour suppressor some fifteen years ago, the transcription factor p53 has attracted paramount attention for its role as “the guardian of the genome”. TP53 mutations occur so frequently in cancer, regardless of patient age or tumour type, that they appear to be part of the life history of at least 50% of human tumours. In most tumours that retain wild-type p53, its function is inactivated due to deregulated HDM2, a protein which binds to p53 and which can inhibit the transcriptional activity of p53 and induce its degradation. RITA is a low-molecular-weight compound which addresses the second group of tumours retaining functionally reactive wt p53. It was found in a screening of the National Cancer Institute (NCI) library of low-molecular-weight compounds based on its ability to selectively kill wtp53-containing cells. RITA binds directly to p53 and diplaces its main destructor Mdm2, as well as inducing a shift in the conformation of p53. This is in contrast to the wtp53-reactivating compound Nutlin3a, which targets Mdm2, inhibiting its ability to degrade p53. Using microarray technology we have explored the effect of RITA on the transcriptome of isogenic cell-lines with knocked-out (KO) or intact (WT) TP53. While the effects on KO cells are below detection limit, the effects on WT cells are profound. The known p53 targets induced are predominately apoptotic, in contrast to the genes affected by Nutlin3a, which are exclusively growth-arrest genes. Keywords: Antitumor agent HCT116 parental and HCT116 p53-null (HCT116 TP53-/-) cells were subjected to treatment with 1uM RITA for 12h, or left untreated. The experiment was done in three independent biological replicates.

2009-02-28 | E-GEOD-11578 | biostudies-arrayexpress

USP15-dependent lysosomal pathway controls p53-R175H turnover in ovarian cancer cells

Project description:Gain-of-function p53 mutants such as p53-R175H form stable aggregates that accumulate in cells and play an important role in cancer progression. Selective degradation of gain-of-function p53 mutants has emerged as a highly attractive therapeutic strategy to target cancer cells harboring specific p53 mutations. We identified a small molecule called MCB-613 to cause rapid ubiquitination, nuclear export, and degradation of p53-R175H through lysosome-mediated pathway leading to catastrophic cancer cell death. In contrast to its effect on the p53-R175H mutant, MCB-613 causes slight stabilization of p53-WT and has weaker effects on other p53 gain-of-function mutants. Using state-of-the-art genetic and chemical approaches, we identified the deubiquitinase USP15 as the mediator of MCB-613’s effect on p53-R175H and established USP15 as a selective upstream regulator of p53-R175H in ovarian cancer cells. These results confirm that distinct pathways regulate the turnover of p53-WT and the different p53 mutants and open new opportunities to selectively target them.

2018-02-07 | GSE110220 | GEO

Effect of wtp53-reactivating drug RITA on HCT116 cells

2009-02-28 | GSE11578 | GEO

Genome profiling of WDR5, P53, H3K4Me3 binding in mouse embryonic bodies using SFEBq differetiation methods

Project description:This study describes the binding profile of WDR5, p53 and H3K4Me3 in mouse embryonic bodies at day 2 (WT, Wdr5 KO, Wdr5 and p53 double knockout)

2019-11-25 | GSE140899 | 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