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SRX835937: GSM1572252: WT mouse PolyA+ RNAseq; Mus musculus; RNA-Seq
1 ILLUMINA (NextSeq 500) run: 52.9M spots, 4G bases, 1.9Gb downloads

Submitted by: Gene Expression Omnibus (GEO)
Study: Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth
show Abstracthide Abstract
We investigated the genomewide binding pattern of prevalent p53 gain-of-function (GOF) mutants by ChIP-seq, in a panel of breast cancer cell lines. We assessed the genomewide changes of H3K4me3 upon GOF p53 knockdown in MDA-MB-468 breast cancer cells bearing the p53 R273H mutation. Overall design: This study uses ChIP-seq of H3K4me3 and histone H3 in wild-type or p53 R172H knock-in MEFs. Additionally, this study examines the transcriptome of wild-type or p53 R172H knock-in MEFs using polyA+ RNA-seq.
Sample: WT mouse PolyA+ RNAseq
SAMN03273078 • SRS813744 • All experiments • All runs
Organism: Mus musculus
Library:
Instrument: NextSeq 500
Strategy: RNA-Seq
Source: TRANSCRIPTOMIC
Selection: cDNA
Layout: SINGLE
Construction protocol: For ChIP-seq, cells were crosslinked with formaldehyde (1% final) for 10min at room temperature, and harvested for sonication. Nuclei were extracted and chromatin was sheared to an average size of 200bp using a Covaris S220 sonicator For RNA-seq, polyA+ RNA was isolated by two rounds of polyA selection using the Life Technologies mRNADirect kit per manufacturer's recommendations. Sequencing libraries for ChIP-seq were constructed using the NEBNext Ultra kit as per manufacturer's recommended instructions. Sequencing libraries for polyA+, stranded-RNA-seq were constructed using the NEBnext Ultra Directional RNAseq kit as per manufacturer's recommended instructions.
Experiment attributes:
GEO Accession: GSM1572252
Links:
External link:
Runs: 1 run, 52.9M spots, 4G bases, 1.9Gb
Run# of Spots# of BasesSizePublished
SRR174843652,925,0634G1.9Gb2015-07-31

ID:
1185712

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