Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-MTAB-10041

ABSTRACT: RNA-seq of mouse colon to investigate how suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity

PROVIDER: E-MTAB-10041 | ExpressionAtlas | 2024-11-14

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-MTAB-10041-analysis-methods.tsv	Tabular
	E-MTAB-10041-analytics.tsv	Tabular
	E-MTAB-10041-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-10041-configuration.xml	Xml
	E-MTAB-10041-g3_g1-mvaPlot.png	Other

Items per page:

1 - 5 of 31

Similar Datasets

RNA-seq of mouse colon to investigate how suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity

Project description:RNA-seq of mouse colon to investigate how suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity

| PRJEB42819 | ENA

Induction of ER stress in HCT116 colon cancer cells

2015-04-01 | GSE63252 | GEO

Induction of ER stress in HCT116 colon cancer cells

Project description:To investigate the role of p53 and DICER in the induction of ER stress, wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells were treated with the ER stress inducers tunicamycin or brefeldin A for 24 hours. Microarray analysis was used to determine changes in gene expression associated with the induction of ER stress, and to compare this induction in wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells Triplicate samples of HCT116 wildtype, HCT116 p53 knockout and HCT116 DICEREX5/EX5 cells were treated with with 0.5 mg/ml of BFA or 2 mg/ml of Tm for 24 h. Following treatment, cells were harvested and lysed in TRIzol reagent and RNA was extracted. Microarray analysis was carried out using Affymetrix HG-U133_Plus-2 arrays.

2015-04-01 | E-GEOD-63252 | biostudies-arrayexpress

E-MTAB-10416

Project description:Suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity

2025-07-07 | E-MTAB-10416 | ExpressionAtlas

Extracts from sweet sorghum (Sorghum bicolor), a feedstock for biorefining, suppressed proliferation and elevated apoptosis in human colon cancer stem cells via suppression of Wnt/beta-catenin signaling pathway

Project description:In colorectal cancer, p53 is commonly inactivated, associated with chemo-resistance, and marks the transition from non-invasive to invasive disease. Cancers, including colorectal cancer, are thought to be diseases of aberrant stem cell populations, as stem cells are able to self-renew, making them long-lived enough to acquire mutations necessary to manifest the disease. We have shown that extracts from sweet sorghum stalk components eliminate colon cancer stem cells (CCSC) in a partial p53-dependent fashion. However, the underlying mechanisms are unknown. In the present study, CCSC were transfected with short hairpin-RNA against p53 (CCSC p53 shRNA) and treated with sweet sorghum phenolics extracted from different plant components (dermal layer, leaf, seed head and whole plant). While all components demonstrated anti-proliferative and pro-apoptotic effects in CCSC, phenolics extracted from the dermal layer and seed head were more potent in eliminating CCSC by elevating caspases 3/7 activity, PARP cleavage, and DNA fragmentation in a p53-dependent and p53-independent fashion, respectively. Further investigations revealed that the anti-proliferative and pro-apoptotic effects were associated with decreases in beta-catenin protein levels, and beta-catenin targets cyclin D1, cMyc, and survivin. These results suggest that the anti-proliferative and pro-apoptotic effects of sweet sorghum extracts against human colon cancer stem cells are via suppression of Wnt/beta-catenin pro-survival signaling in a p53-dependent (dermal layer) and partial p53-independent (seed head) fashion. LCMS used to identify phenolic compounds associated with extract activity

2014-05-01 | MTBLS69 | MetaboLights

LINC01021 attenuates expression and affects alternative splicing of a subset of p53-regulated genes

Project description:Loss of the p53-inducible LINC01021 in p53-proficient CRC cell lines results in increased sensitivity to DNA-damaging chemotherapeutics. Here, we comprehensively analyzed how LINC01021 affects the p53-induced transcriptional program. Using a CRISPR/Cas9-approach we deleted the p53 binding site in the LINC01021 promoter of SW480 colorectal cancer cells and subjected them to RNA-Seq analysis after activation of ectopic p53. RNA affinity purification followed by mass spectrometry was used identify proteins associated with LINC01021.

2024-05-10 | PXD050892 | Pride

Suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity

Project description:Suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity

| PRJEB44756 | ENA

p53 ChIP-seq of primary astrocytes in vitro

Project description:To investigate the transcriptional regulation by p53 in astrocytes, we performed ChIP-sequencing using p53 antibody (Leica CM-5) or rabbit IgG control in wildtype primary mouse cortical astrocytes.

2023-02-23 | GSE196863 | GEO

CFTR is a tumor suppressor gene in murine and human intestinal cancer [microarray]

Project description:Analysis of the cystic fibrosis gene Cftr in the colon and small intestine of Cftr-deficient murine model. The hypothesis was loss of Cftr altered expression of genes important in intestinal homeostasis and oncogenic signaling pathways. The results identified potential roles of Cftr in up- or down-regulating major gene clusters that belong to groups of immune response, ion channel, intestinal stem cell and other growth regulators. Total RNA was isolated from the normal intestine of three Apc wildtype Cftr wildtype and three Apc Cftr-deficient mice. For the colon intestinal epithelia from the same region of the distal colon of each mouse was separated from the rest of the intestine prior to RNA isolation. Therefore RNA was obtained from only epithelial cells. For the small intestine, a section of the mid-duodenum from each mouse was sheared of villi prior to RNA isolation. Therefore RNA was obtained from whole duodenum (minus villi), containing epithelia cells but also stromal and other cells. RNA Seq was then conducted on all samples, with at least two replicates for each biological sample.

2015-12-15 | E-GEOD-75996 | biostudies-arrayexpress

Trancriptome study of zebrafish mutant fn10a

Project description:We conducted functional analysis on zebrafish mutant fn10a by polyA+, 100bp paired end, strand-specific RNA-seq. By comparing the transcriptome of fn10a mutants and their wildtype siblings or wildtype controls, we revealed a transcriptome-wide RNA splicing deficiency and a large amount of intron-retaining transcripts, which resulted in compromised nonsense-mediated RNA decay and activation of the p53 pathway in fn10a mutants. 2 biological replicates were performed to consolidate the findings. We also conducted subcellular RNA-seq between fn10a mutants and wildtype siblings, to investigate the localization of intron retaining transcripts.

2017-02-10 | GSE78106 | GEO

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