Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Genomic location data for ectopic p73 in H1299 lung carcinoma cells

OTHER RELATED OMICS DATASETS IN: GSE11673

PROVIDER: PRJNA109157 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Homo sapiens

Project description:Expression data from p73 over-expression in H1299 cells

| PRJNA109151 | ENA

Transcription profiling by array of human p73 over-expressing H1299 cells

Project description:The integral role of p53 in tumor suppression has promted many laboratories to perform extensive analyses of signaling pathways downstream of the p53 family of sequence-specific DNA binding transcription factors (p53 and its homologs p63 and p73). Despite the ability of p73 to regulate many p53 family target genes, little is known about the specific pathways that modulate p73 during development, tumorigenesis and tumor therapy. In this study we present a gene signature-based approach for connecting signaling pathways to transcription factors, as exemplified by p73. We generated a p73 gene signature by integrating whole-genome chromatin immunoprecipitation and expression profiling. Experiment Overall Design: H1299 lung carcinoma cells were infected with p73 expressing or control adenovirus for 5 h and then harvested.

2008-10-20 | E-GEOD-11626 | biostudies-arrayexpress

iAR22_SARS-CoV-2_scH1299 - cell-type specific constraint-based metabolic models of human H1299 cells with SARS-CoV-2 infection

Project description:A collection of cell-type specific constraint-based metabolic models of human H1299 cells (human non-small cell lung carcinoma cell line) infected with SARS-CoV-2 based that were generated based on gene-expression data.

2025-04-07 | MODEL2311070004 | BioModels

ChIP-Seq of human H1299 lung carcinoma cells - genomic location data for ectopic p73

Project description:The integral role of p53 in tumor suppression has promted many laboratories to perform extensive analyses of signaling pathways downstream of the p53 family of sequence-specific DNA binding transcription factors (p53 and its homologs p63 and p73). Despite the ability of p73 to regulate many p53 family target genes, little is known about the specific pathways that modulate p73 during development, tumorigenesis and tumor therapy. In this study we present a gene signature-based approach for connecting signaling pathways to transcription factors, as exemplified by p73. We generated a p73 gene signature by integrating whole-genome chromatin immunoprecipitation and expression profiling. Experiment Overall Design: H1299 lung carcinoma cells were transduced with TAp73beta or GFP expressing adenoviruses. Microarray analysis (on the GFP and TAp73beta samples) and ChIPSeq analysis (on the TAp73beta sample) were performed to identify candidate p73 target genes.

2009-08-30 | E-GEOD-11672 | biostudies-arrayexpress

Homo sapiens

Project description:Expression data from H1299 human non-small cell lung carcinoma cell lines stably expressing CHES1 compared with H1299 infected with an empty vector

| PRJNA213883 | ENA

Homo sapiens

Project description:Expression data from H1299 and H460 lung cancer cell lines

| PRJNA125307 | ENA

Expression analysis of gene expression chang in Homo sapiens Small cell lung carcinoma cells NCIH446 after knock down Follitin1 gene

Project description:Investigation of whole genome gene expression level changes in a Homo sapiens Small cell lung carcinoma cells NCIH446 after knock down of Follitin1 gene expression

2017-05-27 | GSE99337 | GEO

CIT - Homo sapiens - APUP - Genomic aberrations in Lung Adenocarcinoma in Never Smokers

Project description:41 lung adenocarcinoma from never-smokers hybridized on Illumina SNP arrays on 13 HumanCNV370-Quadv3 chips. High-resolution array comparative genomic hybridization analysis of lung adenocarcinoma in 41 never smokers for identification of new minimal common regions (MCR) of gain or loss. The SNP array analysis validated copy-number aberrations and revealed that RB1 and WRN were altered by recurrent copy-neutral loss of heterozygosity.The present study has uncovered new aberrations containing cancer genes. The oncogene FUS is a candidate gene in the 16p region that is frequently gained in never smokers. Multiple genetic pathways defined by gains of MYC, deletions of RB1 and WRN or gains on 7p and 7q are involved in lung adenocarcinoma in never smokers. A 'Cartes d'Identite des Tumeurs' (CIT) project from the French National League Against Cancer (http://cit.ligue-cancer.net) 41 samples hybridized on Illumina SNP arrays. Submitter : Fabien PETEL petelf@ligue-cancer.net . Project leader : Pr Pierre FOURET pierre.fouret@psl.aphp.fr

2011-07-28 | E-TABM-1169 | biostudies-arrayexpress