Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (ChIP-seq - mus musculus)
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 17 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
- Mus musculus (mouse)
- Samples
- 17 samples: 16 distinct titles, 1 of them repeatedGroups 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
- Loss of BAP1 defines a unique subtype of TP53-mutated de novo AML and confers sensitivity to BCL-xL inhibitorsBlood · 2025
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.
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.
Supplementary files
The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE173547_RAW.tar (it can run to tens of gigabytes).
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.
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 PRJNA726144 and SRA study SRP316872. Searching any of these in the dataset finder brings you back here.
How we read this: Read from 17 sample titles: 16 distinct titles with little repetition. 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.
- GSM5269509 Input_1
- GSM5269510 Input_2
- GSM5269511 TA4191-H3K4me3
- GSM5269512 CL1084-H3K4me3
- GSM5269513 CL1097-H3K4me3
- GSM5269514 CL997-H3K4me3
- GSM5269515 CL1027-H3K4me3
- GSM5269516 TA4191-H3K27me3
- GSM5269517 CL1084-H3K27me3
- GSM5269518 CL1097-H3K27me3
- GSM5269519 CL997-H3K27me3
- GSM5269520 CL1027-H3K27me3
- GSM5269521 TA4191-H2AK119Ub
- GSM5269522 CL1084-H2AK119Ub
- GSM5269523 CL1097-H2AK119Ub
- GSM5269524 CL997-H2AK119Ub
- GSM5269525 CL1027-H2AK119Ub
- GSE171815 Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (RNA-seq - mus musculus) 27 samples shares bap1, tp53, myelo-erythroid, cooperates, deficiency, progenitor, transform
- GSE266948 Loss of BAP1 cooperates with TP53 deficiency to transform a common myelo-erythroid progenitor (scRNA-seq - mus musculus) 10 samples shares bap1, tp53, myelo-erythroid, cooperates, deficiency, progenitor, transform
- GSE279386 Tp53 and Tet2 mutations cooperatively transform progenitors (RNA-Seq) 24 samples shares tp53, progenitor, transform
- GSE329244 Polycomb erasers BAP1 and UTX are dispensable for rapid bivalent gene activation but essential for enhancer establishment [ChIP-seq] 64 samples shares bap1, chip-seq
- GSE121709 Role of BAP1 in pancreatic cancer (ChIP-seq Mus musculus) 14 samples shares bap1, chip-seq
- GSE190901 H3K27ac ChIP-seq analysis of genetically engineered mouse models (GEMMs) of PDA with KRAS and TP53 mutations 12 samples shares tp53, chip-seq
- GSE285355 Tp53 and Tet2 mutations cooperatively transform GMP (RNA-Seq) 12 samples shares tp53, transform
- GSE288819 The tumour suppressor STAG2 cooperates with DREAM to maintain quiescence in the urothelium [ChIP-Seq_NU1] 13 samples shares cooperates, chip-seq
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.