GEO series

The Ashkenazi-centric G334R variant of TP53 is severely impaired for transactivation but retains tumor suppressor function in a mouse model [ChIP-Seq]

GSE277586 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 44 samples Submitted 2025/09/19 Platform GPL30173

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 44 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Homo sapiens (human)
Samples: 44 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.

Summary (written by the submitters)

Mutations in the TP53 tumor suppressor gene are the most abundant genetic occurrences in cancer. Some of these mutations lead to loss of function of p53 protein, some are gain of function, and some variants are hypomorphic (partially-functional). Currently, there is no clinical distinction between different p53 mutations and cancer therapy or prognosis.

Read the full summary ↓

Mutations in the oligomerization domain of p53 appear to be quite distinct in function, compared to mutations in the DNA binding domain. Here we show that, like other p53 oligomerization domain mutants, the Ashkenazi-specific G334R mutant accumulates to very high levels in cells and is significantly impaired for the transactivation of canonical p53 target genes. Surprisingly, we find that this mutant retains the ability to bind to consensus p53 target sites. A mouse model reveals that mice containing the G334R variant show increased predisposition to cancer, but only a fraction of these mice develop cancer at late onset. We show that the G334R variant retains the ability to interact with the SP1 transcription factor and contributes to the transactivation of joint SP1-p53 target genes. The combined evidence indicates that G334R is a unique oligomerization domain mutant that retains some tumor suppressor function.

This dataset

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Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE277586_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1162871 and SRA study SRP533636. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 44 more — browse all 44 samples with per-sample file links →

Datasets on a similar topic

GSE277585 The Ashkenazi-centric G334R variant of TP53 is severely impaired for transactivation but retains tumor suppressor function in a mouse model [RNA-seq] 18 samples shares g334r, tp53, ashkenazi-centric, transactivation, suppressor, severely, impaired
GSE262052 Charting the regulatory landscape of TP53 on transposable elements in cancer [ChIP-seq] 9 samples shares tp53, chip-seq
GSE291035 TP53 missense-specific transcriptional plasticity drives resistance against cell cycle inhibitors in pancreatic cancer [ChIP-Seq] 4 samples shares tp53, chip-seq
GSE198940 Comparative cofactor screens reveal the influence of transactivation domains and core promoters on the mechanisms of transcription [ChIP-seq] 13 samples shares transactivation, chip-seq
GSE262051 Charting the regulatory landscape of TP53 on transposable elements in cancer [ATAC-seq] 24 samples shares tp53
GSE328076 LHX2 drives neuroendocrine transformation in TP53/RB1-deficient prostate cancer 14 samples shares tp53
GSE246044 Chromatin accessibility and transcriptomic responses to HDAC inhibitors in TP53 mutated patient-derived colon cancer organoids [ATAC-seq] 12 samples shares tp53
GSE255000 Chromatin accessibility profiling by ATAC-seq in LNCaP-shNT and LNCaP-shTP53 cells 6 samples shares tp53

Search all human ChIP / ATAC / CUT&Tag datasets in GEO →

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.