Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

13 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq of H1299 cells stably transfected with empty vector or the p53 mutant R273H

ABSTRACT: This experiment was performed to determine which gene promoters mutant p53 binds and transcriptionally regulates in order to understand how mutant p53 accomplishes its gain of function phenotype.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Homo sapiens

SUBMITTER: Sumitra Deb

PROVIDER: E-MTAB-5653 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of H1299 cells stably transfected with empty vector or the p53 mutant R273H.

Project description:This experiment aimed to determine the genes that were upregulated when mutant p53 (R273H) was expressed. We used H1299 lung cancer cells that are endogenously p53-null and overexpressed the p53 mutant.

2017-04-16 | E-MTAB-5652 | biostudies-arrayexpress

RNA-seq of cell lines containing p53-R273H or p53-R273H 22/23

Project description:RNA-sequencing was performed to determine the differences between cells that contain mutant p53 and a transactivation deficient mutant of p53 to determine why the TAD mutant cells don't form tumors.

2020-12-18 | E-MTAB-9833 | biostudies-arrayexpress

Mutant p53R273H regulated microRNA profiling in presence and absence of DNA damage in H1299 cells

Project description:In the present study, we used a high-throughput small RNA deep sequencing followed by a systematic computational analysis to identify genome wide mutant p53R273H regulated miRNAs in both DNA damage dependent and independent context. Several miRNA-mRNA regulatory networks have been predicted that might contribute to mutant p53 GOF properties. Differentially regulated miRNA signature profile has been validated in the lung cancer patients harboring wildtype and mutant p53. We identified specific miRNA signatures for lymph node metastasis associated with p53 mutation in lung adenocarcinoma and also predicted the possible contribution of two mutant p53 regulated miRNAs in EMT process. Furthermore, this study identified a hitherto unknown miRNA in human which might act as one of the crucial downstream targets of GOF mutant p53 to confer oncogenic properties. Determination of mutant p53R273H regulated microRNAs H1299 cells.

2017-04-28 | E-GEOD-68353 | biostudies-arrayexpress

Using ribosome profiling to investigate the effect of p53 on translation in cancer cells

Project description:p53 is deleted or dysfunctional, or develops these features during the course of disease, with a frequency of about 50% in human cancers. This is clinically important because this group of patients respond very poorly to treatment. Our approach to discovering novel biomarkers or targets for therapy for p53 deleted/dysfunctional disease is to find genes that are translationally regulated by p53. The aim of this experiment is to compare translational efficiencies in cancer cells that are p53 WT, p53-/-, or p53 R175H, in response to doxorubicin.

2021-02-22 | E-MTAB-8100 | biostudies-arrayexpress

Human p53 interating protein ID

Project description:Wild type and mutant p53 were transfected in H1299 cells and the associated complexes were affinity purified. The p53 interacting proteins then analyzed by ms/ms.

2019-01-29 | PXD012463 | Pride

H1299 cells: p53 transcriptional response in hypoxia

Project description:Transcriptional profiling of H1299 non-small cell lung carcinoma cells transfected with either wt p53 or mut(175) p53 driven by the 5xHRE promoter (5 repeats of hypoxia-inducible factor response elements) and treated for 16 h with normoxia (21% O2) or hypoxia(<0.1% O2). 5xHRE promoter ensures that p53 expression is induced in hypoxic conditions only. Goal was to determine the transcriptional response of p53 in hypoxia and the 175 p53 mutant was used as a control as it is DNA-binding defective and transcription-incompetent mutant. Four-condition experiment: wt p53-transfected H1299 cells treated with normoxia, mut p53-transfected H1299 cells treated with normoxia, wt p53-transfected H1299 cells treated with hypoxia, mut p53-transfected H1299 cells treated with hypoxia. Biological replicates: 1 normoxic sample with wt p53, 1 normoxic sample with mut p53, 3 hypoxic samples with wt p53, 3 hypoxic samples with mut p53.

2014-01-08 | E-GEOD-53893 | biostudies-arrayexpress

Distinct gain of function mechanism for the hot-spot mutant p53R175H

Project description:TP53 (p53) is the most commonly mutated gene in human cancers, and p53 missense mutations are present in more than 40% of all human tumors. Most p53 mutations are located within the DNA binding domain, including hotspot mutations R175H, R248W, and R273H. To elucidate the precise mechanism by which p53 missense mutants execute their gain-of-functions (GOFs) in vivo, we used a proteomic screen to identify any protein that recognizes the p53 DNA-binding domain (DBD) in a manner dependent on its mutation status. To do so, we first purified the potential binding proteins associated with the p53 DBD through multi-step affinity chromatography from a SFB-p53 H1299 stable cell line. The affinity-purified SFB-p53 interacting proteins were detected by liquid chromatography mass spectrometry/mass spectrometry (LC–MS/MS) and revealed a few cellular proteins that have been reported to interact with the DNA binding domain of p53, such as TP53BP1, USP28, and Sirt1. Interestingly, we also identified many new interacting proteins from the same complex.

2023-02-17 | PXD039886 | Pride

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

Coupling p53 binding and nucleosome occupancy measurements at p53 binding sites

Project description:We were interested to explain why p53 binds some high affinity sites in contrast to other high affinity sites that are not bound by p53. p53 binding was measured using p53 ChIP-CHIP and in parallel nucleosome occupancy was measured on these same sites Comparison between p53 binding and nucleosome occupancy at p53 predicted binding sites ChIP-CHIP of p53 from MCF7EcoR under Basal conditions and MCF7EcoR treated with NCS (Activated) and Mononucleosomal extraction from MCF7sip53, MCF7EcoR under Basal conditions and MCF7EcoR treated with NCS (Activated) Expression analysis of MCF7sip53 and MCF7EcoR treated with NCS (Activated)

2010-08-09 | E-GEOD-22783 | 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

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