GEO series

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

GSE277585 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2025/09/19 Platform GPL30173

At a glance

RNA-seq (gene expression) · human · 18 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Homo sapiens (human)
Samples: 18 samples: 6 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
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.
Paper: The Ashkenazi-Centric G334R Variant of TP53 is Severely Impaired for Transactivation but Retains Tumor Suppressor Function in a Mouse ModelMolecular and cellular biology · 2024

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.

Published in

The Ashkenazi-Centric G334R Variant of TP53 is Severely Impaired for Transactivation but Retains Tumor Suppressor Function in a Mouse Model

Stieg DC, Casey K, Karisetty BC et al. · Molecular and cellular biology 2024 · PMID 39520074 · doi:10.1080/10985549.2024.2421885

This dataset

Open GSE277585 in finder → Find more human RNA-seq datasets →

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 GSE277585_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1162881 and SRA study SRP533640. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39520074) ↗

Study design

6 conditions, mostly in triplicate

HCT-WT-Control ×3 HCT-WT-6h ×3 HCT-WT-24h ×3 HCT-G334R-Control ×3 HCT-G334R-6h ×3 HCT-G334R-24h ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 sample titles; they account for 18 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM8525068 HCT-WT-Control-1 HCT-WT-Control
GSM8525069 HCT-WT-Control-2 HCT-WT-Control
GSM8525070 HCT-WT-Control-3 HCT-WT-Control
GSM8525071 HCT-WT-6hr-1 HCT-WT-6h
GSM8525072 HCT-WT-6hr-2 HCT-WT-6h
GSM8525073 HCT-WT-6hr-3 HCT-WT-6h
GSM8525074 HCT-WT-24hr-1 HCT-WT-24h
GSM8525075 HCT-WT-24hr-2 HCT-WT-24h
GSM8525076 HCT-WT-24hr-3 HCT-WT-24h
GSM8525077 HCT-G334R-Control-1 HCT-G334R-Control
GSM8525078 HCT-G334R-Control-2 HCT-G334R-Control
GSM8525079 HCT-G334R-Control-3 HCT-G334R-Control
GSM8525080 HCT-G334R-6hr-1 HCT-G334R-6h
GSM8525081 HCT-G334R-6hr-2 HCT-G334R-6h
GSM8525082 HCT-G334R-6hr-3 HCT-G334R-6h
GSM8525083 HCT-G334R-24hr-1 HCT-G334R-24h
GSM8525084 HCT-G334R-24hr-2 HCT-G334R-24h
GSM8525085 HCT-G334R-24hr-3 HCT-G334R-24h

Datasets on a similar topic

GSE277586 The Ashkenazi-centric G334R variant of TP53 is severely impaired for transactivation but retains tumor suppressor function in a mouse model [ChIP-Seq] 44 samples shares g334r, tp53, ashkenazi-centric, transactivation, suppressor, severely, impaired, variant
GSE311354 A personalized therapeutic approach for cancer containing the African-centric P47S variant of TP53 18 samples shares tp53, variant
GSE272900 RNA variant assessment using transactivation and transdifferentiation 16 samples shares transactivation, variant
GSE245163 A p53 score derived from TP53 CRISPR/Cas9 HMCLs predicts survival and reveals major role of BAX in BH3 mimetics response 138 samples shares tp53
GSE245162 A p53 score derived from TP53 CRISPR/Cas9 HMCLs predicts survival and reveals major role of BAX in BH3 mimetics response [2] 96 samples shares tp53
GSE306117 Distinct genomic and immunologic tumor evolution in germline TP53-driven breast cancers 74 samples shares tp53
GSE262053 Charting the regulatory landscape of TP53 on transposable elements in cancer [RNA-seq] 72 samples shares tp53
GSE301195 Ubiquitin specific peptidase 7 promotes TP53 mutant malignancy by deubiquitinating and stabilizing DDR1 60 samples shares tp53

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