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Efferocytosis induces proangiogenic function and chromatin remodeling in tumor-associated macrophages [ATAC-seq]

GSE306916 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/06/05 Platform GPL30172
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 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
12 samples: 12 samples, each with a distinct title — no replicated groupsGroups 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)
Macrophages remove apoptotic cells by efferocytosis during immune-surveillance and in the tumor microenvironment (TME). However, the gradual molecular and epigenetic consequences of efferocytosis on the single macrophage are not thoroughly elucidated. Here we introduce Effero-seq, an approach that captures single-cell transcriptomic changes coupled with lysosomal acidification tracked by pHrodo, thus enabling the dissection of molecular dynamics over time following engulfment.
Read the full summary ↓
Using apoptotic pHrodo-labeled cells as cargo, we defined the effero-score, a gene program gradually upregulated correlatively with pHrodo intensity. In a murine melanoma model, we found that efferocytosis induces a pro-angiogenic function in macrophages with spatial proximity to vascular niches. Moreover, efferocytosis reprograms chromatin accessibility, leading to attenuated macrophage response to IFNγ. In human uveal melanoma, expression of the effero-score is correlated with poor survival. Effero-seq sheds light on the molecular reprogramming induced by efferocytosis in the TME, opening new avenues for understanding macrophage function and developing targeted treatments.
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 GSE306916_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 PRJNA1313924 and SRA study SRP616675. Searching any of these in the dataset finder brings you back here.

Study design
12 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 12 sample titles: 12 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

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