Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The DNA binding selectivity by wild-type p53 and PANDAs

ABSTRACT: We performed ChIP-seq analysis of p53-null HCT116 cells stably expressed wild-type p53 or mutant p53 followed by ATO treatment (PANDAs) to identify p53 binding characteristics by wild-type p53 and PANDAs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE195622 | GEO | 2024/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome-wide expression analysis of wild-type p53 and PANDAs in p53-null HCT116 cells

Project description:Our RNA-seq data suggested the different transcriptional profiles of wild-type p53 and PANDAs treated with or without ATO.

2024-01-31 | GSE206395 | GEO

RNAseq analysis for transcriptomes of ATO treated U937 cell lines expressing 10 type 1 p53 mutants, type-3 p53-R273H, p53 null, or p53 wild-type

Project description:To globally evaluate to what extend type-1 p53 mutant transcription activity can be restored by arsenic trioxide (ATO) (compared to wild-type p53), p53-null U937 cells introduced with 10 frequent type-1 p53, type-3 p53-R273H (negative control), empty vector or wild-type p53 were treated with or without 1 μg/mL ATO. mRNA was isolated and then subject to deep sequencing, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed using Cutadapt. Results and conclusions: The type-1 p53 mutants are the major cellular targets of ATO in the current cell contexts. The expression profiles of well-established p53 targets in cells expressing wild-type p53 highly correlated with the ones in cells expressing ATO-rescued type-1 mutants, but not those in cells expressing ATO-treated R273H. In cells harboring type-1 mutants, the median expression levels of these targets were elevated by ATO to extents comparable to wild-type p53.

2024-08-01 | GSE182565 | GEO

RNAseq analysis for transcriptomes of ATO treated U937 cell lines expressing p53-R280I or p53 wild-type

Project description:To globally evaluate to what extend the p53 mutant transcription activity can be restored by arsenic trioxide (ATO), p53-null U937 cells introduced with p53-R280I or wild-type p53 were treated with or without 1 μg/mL ATO. mRNA was isolated and then subject to deep sequencing, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed using Cutadapt.

2024-08-01 | GSE213678 | GEO

RNAseq analysis for transcriptomes of ATO+DAC treated THP-1cell lines expressing p53-R282W or p53 wild-type

Project description:To globally evaluate to what extend the p53 mutant transcription activity can be restored by arsenic trioxide (ATO) and decitabine (DAC) co-treatment, p53-null THP-1 cells introduced with p53-R282W or wild-type p53 were treated with ATO (1 μg/ml) and DAC (5 μM). mRNA was isolated and then subject to deep sequencing, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed using Cutadapt.

2024-07-31 | GSE269126 | GEO

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.

2010-07-31 | GSE17472 | GEO

Identification of p53-regulated genes in wild-type p53 or p53-null HCT116 cells

Project description:Identification of p53-regulated genes in wild-type p53 or p53-null HCT116 cells

| PRJNA517505 | ENA

TP53 wild type cells are resistant to arsenic trioxide induced dynamic transcriptional changes

Project description:Previous and our results show that cells with mutant p53 are more sensitive to arsenic trioxide (ATO) induced cell growth inhibition. To explore the underling mechanisms, we conduct a detailed analysis of the globe transcriptional profiles of ATO regulated genes in breast, colon and lung cancer cells with different p53 status. We find p53 wild type cells are resistant to ATO induced globe dynamic transcriptional changes, thus resistant to ATO induced cell growth inhibition. P53 inhibitor PFTα releases p53 mediated transcriptional resistance and increases the sensitivity of ATO in p53 wild type tumor cells.

2020-12-31 | GSE124347 | GEO

Identification of arsenic trioxide (ATO)-rescuable p53 mutations and temperature-sensitive p53 mutations in p53-null U937 cells using a patient-derived 800 p53 mutation library

Project description:Thousands of diverse p53 mutations have been identified in cancer. The leukemia-treating drug arsenic trioxide (ATO) rescues a part of p53 mutations with high potency. To repurpose ATO in personalized p53-targeted therapy, here we quantitatively determined the frequent 800 p53 mutations, covering 95.8% p53 missense-mutation cases in cancer, for their rescue potencies of cell growth inhibitory activity and mouse tumor suppressive activity by ATO. Furthermore, we determined the temperature sensitivity of 800 mutations in mammalian U937 cells and founded that ATO preferentially rescued temperature-sensitive subtype of structural p53 mutants.

2024-08-01 | GSE182927 | GEO

Identification of Genes Preferentially Required for Growth of p53-Deficient Human Cancer Cells

Project description:We describe a synthetic interaction screen to identify genes preferentially required for proliferation of p53-deficient human cancer cells. An isogenic pair of p53+/+ and p53-/- human colorectal HCT116 cell lines was stably transduced with a short hairpin RNA (shRNA) library encoded by lentiviruses that integrate in the genomic DNA of the host. Comparison of the frequency of each type of integrated lentivirus in the 2 cell types at an early time point (40hrs) and after about 12 mitotic cycles (10days), reveals genes whose knockdown preferentially impaired growth of p53-/- or p53+/+ HCT116 cells. Keywords: Functional Genomics

2010-05-01 | GSE15967 | GEO

BRD4 inhibitor JQ1 increase the sensitivity of arsenic trioxide in pancreatic cancer

Project description:Pancreatic cancer is a deadliest type of malignancy, largely due to lack of effective intervention. We here report a pair of agents, ATO and JQ1, which synergistically induce apoptosis in the malignancy. Through global and molecular approaches, we have provided evidence that these agents are both able to modulate ER stress and autophagy in the cancer, probably acting in different ways. Cross-talks between ER stress and autophagy are implicated during ATO/ATO plus JQ1 induced apoptosis, in which NRF2 appears to play a central role. of the globe transcriptional profiles of ATO regulated genes in breast, colon and lung cancer cells with different p53 status. We find p53 wild type cells are resistant to ATO induced globe dynamic transcriptional changes, thus resistant to ATO induced cell growth inhibition. P53 inhibitor PFTα releases p53 mediated transcriptional resistance and increases the sensitivity of ATO in p53 wild type tumor cells.

2019-12-31 | GSE124069 | 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