← BioTransfer GEO Dataset Finder
GEO series

AKAP95 condensates regulate transcription and can be targeted in MLL-fusion driven oncogenesis (ChIP-Seq)

GSE271854 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 23 samples Submitted 2025/11/11 Platform GPL34281Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 23 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
23 samples: 21 distinct titles, 2 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.
Summary (written by the submitters)
Oncogenic transcription represents a crucial event in MLL rearranged (MLLr) leukemia, yet the precise role of transcription co-activators in MLL-fusion protein-associated transcription and their contribution to leukemogenesis remain incompletely understood. Here, we demonstrate that AKAP95 is notably up-regulated in both MLLr patients and in MLL-AF9-transformed mouse bone marrow.
Read the full summary ↓
AKAP95 proves essential for initiating mouse MLL-AF9 leukemia, exhibiting widespread DNA binding across the genome, particularly at gene promoters. Interaction with the translocated MLL1 fragment primarily occurs through phase separation mechanisms. AKAP95's RNA-binding properties, coupled with its phase separation behavior, govern its binding to pre-mRNA and concurrent transcriptional regulation. Importantly, we engineered a peptide to disrupt its phase separation, effectively attenuating AKAP95-mediated transcriptional co-activation and inhibiting the growth of MLLr cell lines. These findings illustrate a vivid example of an RNA-binding protein orchestrating transcription and tumorigenesis via phase separation, underscoring the potential for targeting oncogenic condensation mechanisms therapeutically.
This dataset
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.

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 GSE271854_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1133759 and SRA study SRP518850. Searching any of these in the dataset finder brings you back here.

Study design
21 distinct titles, 2 of them repeated
WT_H3K4Me ×2 KO_H3K4Me ×2

How we read this: Read from 23 sample titles: 21 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.

Samples in this study
Datasets on a similar topic

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

Share this dataset

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.