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

Human BJ fibroblasts containing control vs. BRD7 shRNA

ABSTRACT: Transcriptional profiling of human BJ fibroblasts comparing control FF shRNA expressing cells vs. BRD7 shRNA expressing cells under two conditions, either untreated or treated with 8uM nutln-3a for 8 hours. This experiment was done using two independent shRNAs targeting BRD7. Nutlin-3a was used to stabilize p53 and induce its transcriptional activity. Two-condition experiment, FF shRNA cells vs. BRD7 shRNAs cells in two experimental conditions, either untreated or treated with nutlin-3a.

ORGANISM(S): Homo sapiens

SUBMITTER: Anna Burrows

PROVIDER: E-GEOD-22607 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Polybromo-associated BRG1-associated factor components BRD7 and BAF180 are critical regulators of p53 required for induction of replicative senescence.

Burrows Anna E AE Smogorzewska Agata A Elledge Stephen J SJ

Proceedings of the National Academy of Sciences of the United States of America 20100726 32

A variety of tumor-suppressor mechanisms exist to promote genome integrity and organismal survival. One such mechanism is cellular senescence. In response to replicative aging, DNA damage, and oncogenic stimuli, the p53 and Rb pathways are activated to prevent the proliferation of damaged cells by inducing senescence or apoptosis. We have performed a loss-of-function genetic screen in primary human cells to identify components of the senescence machinery. Here we describe BRD7 and BAF180 as uniq ...[more]

PMID: 20660729

Similar Datasets

Expression data from human sarcoma patient samples treated with either vehicle control or Nutlin-3a

Project description:This study has examined the molecular mechanisms underlying sensitivity of sarcomas to Nutlin-3a, a non-genotoxic activator of the p53 pathway. Human patient material was collected immediately following surgical resection, dissected into small pieces and ex planted onto gelatin sponges immersed in media containing either vehicle control or Nutlin-3a (10uM and/or 50uM) for 48 hours. Nutlin-3a represents a novel targeted therapy for the treatment of sarcomas. We have examined expression profiles of genes upregulated in sarcoma patient derived tissues following nutlin-3a treatment ex vivo 16 samples ((Vehicle control and Nutlin-3a (10uM and 50uM) treated samples)) from 6 sarcoma patients

2014-03-10 | E-GEOD-48296 | biostudies-arrayexpress

Human BJ fibroblasts containing control vs. BRD7 shRNA

Project description:Transcriptional profiling of human BJ fibroblasts comparing control FF shRNA expressing cells vs. BRD7 shRNA expressing cells under two conditions, either untreated or treated with 8uM nutln-3a for 8 hours. This experiment was done using two independent shRNAs targeting BRD7. Nutlin-3a was used to stabilize p53 and induce its transcriptional activity.

2010-07-01 | GSE22607 | GEO

MicroRNA profiling by array of human multiple myloma p53 wild type cells treated with nutlin 3A

Project description:The miRNA profiles were analyzed for nutlin 3A treated and untreated multiple myloma p53 wild type cells

2010-07-22 | E-TABM-1038 | biostudies-arrayexpress

Discovery of the p53 targetome in MCF7 cells from RNA-seq data

Project description:RNA-seq and ChIP-seq on MCF-7 breast cancer cell line upon activation of p53 by the non-genotoxic small molecule Nutlin-3a RNA-seq on MCF7 without (NS) or with Nutlin-3a stimulation (S), in duplicate, using illumina HiSeq 2000

2014-05-27 | E-GEOD-47042 | biostudies-arrayexpress

Discovery of the p53 targetome in MCF7 cells from ChIP-Seq data

Project description:RNA-seq and ChIP-seq on MCF-7 breast cancer cell line upon activation of p53 by the non-genotoxic small molecule Nutlin-3a ChIP-seq on p53 in MCF7 with Nutlin-3a stimulation (S) in triplicate, and the control (input), in stimulated and non stimulated, using illumina HiSeq 2000

2014-05-27 | E-GEOD-47041 | biostudies-arrayexpress

Global analysis of p53-regulated transcription reveals its direct targets and unexpected regulatory mechanisms (GRO-Seq)

Project description:GRO-seq of HCT116 cells treated with Nutlin to activate p53 HCT116 cells were treated with Nutlin or DMSO for 1 hour

2014-05-15 | E-GEOD-53964 | biostudies-arrayexpress

GSK-3A and GSK-3B knockdown in AML cell lines

Project description:Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6). Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetic-based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3A (GSK-3A) in AML by performing two independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3A induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3AM-bM-^@M-^Sspecific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3B has been well studied in cancer development, these studies support a role for GSK-3A in AML. The AML cell lines, MOLM-14, U937, THP-1 and HL-60, were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), and two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6).

2012-02-27 | E-GEOD-35200 | biostudies-arrayexpress

ChipSeq of mouse embryonic fibroblasts from conditional knock-in mouse carrying a phosphorylation-deficient S180A (SA) mutation in exon 5 of the endogenous mouse Trp53 gene locus

Project description:The mouse S180A (SA) mutation of the Trp53 is a p53 phosphorylation-deficient mutant protein with native conformation. Here we want to assess the impact of DNA binding site phosphorylation of the p53 target gene spectrum and transcriptional activity under untreated conditions and following p53 stabilization with the Mdm2 inhibitor nutlin-3a.

2020-06-04 | E-MTAB-9170 | biostudies-arrayexpress

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:Mice with colonic tumors (chemically induced by AOM/DSS) were treated with Nutlin or control vehicle solution to analyze p53 target gene expression in vivo.

2021-04-20 | E-MTAB-10041 | biostudies-arrayexpress

ChipSeq of conditional knock-in mouse carrying the R178E (EE) mutation in exon 5 of the endogenous mouse Trp53 gene locus.

Project description:The mouse R178E (EE) mutation of the Trp53 is a p53 mutant protein with native conformation that lacks the ability to form tetramers and thus constitutes a mutant form of p53 that lacks DNA binding cooperativity. Here we want to assess DNA binding ability of the EE mutant in MEFs under untreated conditions and following p53 stabilization with the Mdm2 inhibitor nutlin-3a and compare it to p53 KO and WT mice.

2019-09-03 | E-MTAB-6793 | 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