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SLX4IP limits replication stress globally and at ALT telomeres

GSE298728 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2026/05/08 Platform GPL30882
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 16 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
16 samples: 2 × U2OS, SLX4IP, untreated, Biol. RepA, techn vs 2 × U2OS, SLX4IP, untreated, Biol. RepB, techn vs 2 × HEK, SLX4IP, untreated, Biol. RepA, techn vs 2 × HEK, SLX4IP, untreated, Biol. RepB, technGroups 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
SLX4IP limits replication stress globally and at ALT telomeresThe EMBO journal · 2026
Summary (written by the submitters)
Faithful DNA replication is essential for genome stability, yet replication forks face constant stress. The Bloom syndrome helicase (BLM) safeguards fork integrity, but excessive BLM activity can itself induce replication stress. We identify SLX4IP as a genome-wide regulator that restrains BLM to maintain replication fork stability. SLX4IP localizes broadly across chromatin with recruitment enhanced under replication stress.
Read the full summary ↓
Loss of SLX4IP slows replication forks, remodels the replisome, and generates post-replicative single-stranded DNA gaps that are accompanied by elevated nuclear ADP ribose, reflecting compromised replication integrity. These defects are driven by dysregulated BLM activity, establishing SLX4IP as a negative regulator of BLM-dependent replication stress. At ALT telomeres, SLX4IP deficiency triggers ATR signaling, telomere fragility, and accumulation of ALTassociated PML bodies. Here, SLX4IP functions in parallel with FANCM to restrain BLM at ALT telomeres, with co-depletion of SLX4IP and FANCM causing synthetic lethality in ALT-positive cells, a phenotype fully rescued by BLM loss. Together, our results define SLX4IP as a critical genome-wide regulator of replication fork integrity and reveal SLX4IP as a potential vulnerability in ALTpositive cancers.
Published in
SLX4IP limits replication stress globally and at ALT telomeres
Spindler J, Pandolfo F, Koch AE et al. · The EMBO journal 2026 · PMID 42098304 · doi:10.1038/s44318-026-00790-4
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 GSE298728_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 PRJNA1271019 and SRA study SRP589281. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42098304) ↗
Study design
2 × U2OS, SLX4IP, untreated, Biol. RepA, techn vs 2 × U2OS, SLX4IP, untreated, Biol. RepB, techn vs 2 × HEK, SLX4IP, untreated, Biol. RepA, techn vs 2 × HEK, SLX4IP, untreated, Biol. RepB, techn

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 8 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
Datasets on a similar topic

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