Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect on gene expression by p53 family members and the knockdown of AKR1B10

ABSTRACT: To evaluate the effect on gene expression by p53 family members and AKR1B10, we overexpressed p53 family members in H1299 cells or knocked down AKR1B10 in HCT116 cells and evaluated the gene expression by microarray analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47096 | GEO | 2013/10/31

SECONDARY ACCESSION(S): PRJNA203547

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The effect on gene expression by p53 family members and the knockdown of AKR1B10

Project description:To evaluate the effect on gene expression by p53 family members and AKR1B10, we overexpressed p53 family members in H1299 cells or knocked down AKR1B10 in HCT116 cells and evaluated the gene expression by microarray analysis. Gene expression was measured in H1299 cells infected with adenovirus expressing p53, p63g and p73b, and in HCT116 cells transfected with siRNAs targeting AKR1B10 and then treated with adriamycin.

2013-10-31 | E-GEOD-47096 | biostudies-arrayexpress

The effect on lincRNA expression by p53 family members.

Project description:To evaluate the effect on lincRNA expression by p53 family members, we overexpressed p53 family members in H1299 cells and evaluated the lincRNA expression by microarray analysis. lincRNA expression was measured in H1299 cells infected with adenovirus expressing LacZ, p53, p63a, p63g, p73a and p73b.

2014-02-05 | E-GEOD-52739 | biostudies-arrayexpress

The effect on lincRNA expression by p53 family members.

2014-02-05 | GSE52739 | GEO

p53 family members in myogenic differentiation and rhabdomyosarcoma development

Project description:The p53 family comprises the tumor suppressor p53 and the structural homologs p63 and p73. How the three family members cooperate in tumor suppression remains unclear. Here, we report different but complementary functions of the individual members for regulating retinoblastoma protein (RB) function during myogenic differentiation. Whereas p53 transactivates the retinoblastoma gene, p63 and p73 induce the cyclin-dependent kinase inhibitor p57 to maintain RB in an active, hypophosphorylated state. DeltaNp73 inhibits these functions of the p53 family in differentiation control, prevents myogenic differentiation, and enables cooperating oncogenes to transform myoblasts to tumorigenicity. DeltaNp73 is frequently overexpressed in rhabdomyosarcoma and essential for tumor progression in vivo. These findings establish differentiation control as a key tumor suppressor activity of the p53 family. Keywords: oligonucleotide

2006-10-16 | GSE5447 | GEO

Expression profile of HCT116 p53+/+ and P53-/- cells treated with Leptomycin B

2010-07-31 | GSE17472 | GEO

Transcription profiling of human H1299 cellls transformed with different p73/p53 constructs shows C-terminal diversity within the p53 family accounts for differences in DNA binding and transcriptional activity

Project description:The p53 family is known as a family of transcription factors with functions in tumor suppression and development. Whereas the central DNA binding domain is highly conserved among the three family members p53, p63 and p73, the C-terminal domains (CTDs) are diverse and subject to alternative splicing and post-translational modification. Here we demonstrate that the CTDs strongly influence DNA binding and transcriptional activity. While p53 and the p73 isoform p73ï§ have basic CTDs and form weak sequence-specific protein-DNA complexes, the major p73 isoforms ï¡, ï¢ and ï¤ have neutral CTDs and bind DNA strongly. A basic CTD has been previously shown to enable sliding along the DNA backbone and to facilitate the search for binding sites in the complex genome. Our experiments, however, reveal that a basic CTD also reduces protein-DNA complex stability, intranuclear mobility, promoter occupancy in vivo, transgene activation and induction of cell cycle arrest or apoptosis. A basic CTD in p53 and p73ï§ therefore provides both positive and negative regulatory functions presumably to enable rapid switching of protein activity in response to stress. In contrast, most p73 isoforms exhibit constitutive DNA binding activity consistent with a predominant role in developmental control. Experiment Overall Design: Infection of H1299 cell with different p73/p53 constructs by adenoviral system

2008-10-18 | E-GEOD-8660 | biostudies-arrayexpress

Transcription profiling of DeltaNp73 alpha expressing C2C12 myoblasts examined 6 and 24 hours after shifting the cells to a differentiation medium to study the functions of the individual members of P53 family.

2007-11-22 | E-GEOD-5447 | biostudies-arrayexpress

Expression profile of HCT116 p53+/+ and P53-/- cells treated with Leptomycin B

Project description:HCT116 wild type cells express p53. The isogenic HCT116 p53KO cells have the p53 gene knocked out. Cells were treated for 16 hours. Dosages for leptomycin B treatment was 2 nM and 20 nM. Measuring the gene expression profile of the isogenic cell lines when the cells were treated with leptomycin B at different concentrations

2010-07-30 | E-GEOD-17472 | biostudies-arrayexpress

Exosomes of p53 mutant H1299 cells

Project description:Proteome of exosomes purified from H1299-p53R273H (mutant) and H1299-p53-/- cells, which found the levels of Podocalyxin altered in p53-mutant cells.

2018-12-04 | PXD011241 | Pride

p53 and 5hmC in gene regulation

Project description:p53 is one of the most frequently mutated genes in human cancers, which could regulate multiple target genes involved in a widespread of cellular processes. The regulation of DNA methylation dynamics is critical for maintaining genome stability and proper gene expression. Recently a family of Ten-Eleven-Translocation (TET) proteins has been shown to possess the enzymatic activity to oxidize 5mC to 5hmC, and contribute to DNA demethylation. Here we explore the relationship between p53 binding, 5hmC modification and gene activation using human p53-deficient cells (H1299). H1299 Cells with and without p53

2016-04-01 | E-GEOD-53895 | biostudies-arrayexpress

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