Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sex and mutation specific p53 gain-of-function activity in gliomagenesis

ABSTRACT: Sex and mutation specific p53 gain-of-function activity in gliomagenesis

PROVIDER: PRJNA779976 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16931900_1.fastq.gz	Fastqsanger.gz
	SRR16931900_2.fastq.gz	Fastqsanger.gz
	SRR16931901_1.fastq.gz	Fastqsanger.gz
	SRR16931901_2.fastq.gz	Fastqsanger.gz
	SRR16931902_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 108

Similar Datasets

Sex and mutation specific p53 gain-of-function activity in gliomagenesis [ChIP-seq]

Project description:Sex and mutation specific p53 gain-of-function activity in gliomagenesis [ChIP-seq]

| PRJNA779981 | ENA

Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

Project description:Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

| PRJNA779980 | ENA

Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

Project description:The goal of this study is to compare the sex specific effects of the expression of p53 missense mutations on the transcriptomes of male and female primary astrocytes. Primary cortical astrocytes harboring a single floxed Trp53 allele were harvested from male and female postnatal day one pups, and transduced with mutant p53;IRES GFP followed by CRE recombinase. mRNA was collected from male and female astrocytes transduce with mouse Trp53:R172H, Trp53:Y202C, or Trp53:Y217C. This study revealed sex specific gain-of-function effects on the transcriptomes of each cell line that correlated with cancer pathways.

2021-11-16 | GSE188709 | GEO

Sex and mutation specific p53 gain-of-function activity in gliomagenesis [ChIP-seq]

Project description:ChIP-seq analysis of Primary cortical astrocytes harboring a single floxed Trp53 allele harvested from male and female postnatal day one pups, and transduced with mutant p53;IRES GFP followed by CRE recombinase. p53 protein was immunoprecipated from fixed whole chromatin from cells expressing one of three mutants or p53 KO control.

2021-11-16 | GSE188708 | GEO

Sex and mutation specific p53 gain-of-function activity in gliomagenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-11-16 | GSE188710 | GEO

Differential gain-of-function activity of three p53 hotspot mutants in vivo

Project description:To identify mutant p53 gain-of-function, primary murine osteosarcomas expressing p53 heterozygous mutants were compared to p53 heterozygous tumors. Transcriptomes regulated by different p53 hotspots were used to identify their mechanisms of action. Validation was done in cell line expressing mutant p53, to confirm its binding to transcription factors Stat3 and Egr1.

2022-03-23 | GSE198802 | GEO

Proline 152 mutation in p53 abolishes cognate DNA binding, induces gain of function tumorigenesis

Project description:We have identified a relatively rare mutation in p53 in an Indian oral cancer patient sample at the fade end of its DNA binding domain [P152L]. Although P152L p53 DBD potentially binds to DNA, the full length protein is completely devoid of cognate site DNA binding ability. Also the mutant protein can efficiently tetramerize. Significantly, this mutant was found to induce cell mobility and proliferation with greater tumorigenic potential in nude mice, the mechanistic details of which is also investigated upon. These data establish P152L as a new gain of function p53 mutation

2019-08-02 | GSE119654 | GEO

Differential gain-of-function activity of three p53 hotspot mutants in vivo

Project description:Differential gain-of-function activity of three p53 hotspot mutants in vivo

| PRJNA816907 | ENA

26S proteasome is conserved, therapeutically relevant mediator of mutant p53 gain-of-function in cancer

Project description:Mutant p53 proteins, resulting form frequent TP53 tumor suppressor missense mutations, possess gain-of-function activities and are among the most widespread and robust oncoproteins in human tumors. They are potentially important but understudied therapeutic targets. No studies to date have distinguished common, therapeutically relevant mutant p53 gain-of-function effects, from effects specific to different mutant variants and cell backgrounds. Here we identify 26S proteasome machinery as the common downstream effector controlled by mutant p53s in Triple Negative Breast Cancer (TNBC - aggressive carcinomas with TP53 as the most frequently mutated locus) and conserved in other human cancers. We have identified this pathway using a combination of single-model, multi-method vertical analysis (whole cell proteome, RNA sequencing an ChIP sequencing) and multi-cell line, horizontal analysis of transcriptiomes. We found that different missense mutant p53s regardless of the cell background transcriptionaly activate whole 26S proteasome machinery. Proteasome activity is significantly increased in p53 mutant versus wild-type or knockdown/null status - in cellular and mouse models as well as in human breast tumors. Increased proteasome activity leads to inhibition of tumor suppressive pathways. The control of mutant p53 over proteasome transcription and activity results in the increased resistance to proteasome inhibitors. By combining the mutant p53 targeting agents and proteasome inhibitor we were able to overcome the “bounce-back” proteasome inhibitor resistance mechanism in mutant p53 bearing TNBC cells and xenografts in vivo.

2016-05-03 | PXD001673 | Pride

Expression data from salivary tumor tissues derived from MMTV-ras transgenic mice with wild-type p53, no p53 or gain-of-function mutant p53

Project description:Salivary tumors isolated from MMTV-ras transgenic mice expressing wild-type p53, no p53 or p53R172H gain-of-funcion mutant were subjected to genome-wide gene expression profiling to assess the effect of the different p53 status on tumor gene expression.

2014-08-15 | GSE59452 | 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