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MED16 negatively regulates erythropoiesis and myelopoiesis through modulation of chromatin accessibility [ChIP-Seq human]

GSE248804 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2025/01/01 Platform GPL20795
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 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
Homo sapiens (human)
Topic
Myelodysplastic syndromesThis series is part of our curated briefing on it.
Samples
12 samples: 6 conditions, mostly in duplicateGroups 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)
The Mediator complex plays a crucial role in regulating gene expression by interacting with transcription factors. In this study, we investigated the function of MED16, a core member of the tail module of the Mediator complex, in hematopoietic development. Our findings reveal that MED16 serves as a critical modulator of hematopoiesis by controlling chromatin accessibility at specific target genes.
Read the full summary ↓
Loss of MED16 leads to a shift towards erythropoiesis and myelopoiesis in both human and mouse models. We found that MED16 deficiency increases chromatin accessibility at the RUNX1-binding promoter, promoting the expression of erythroid and innate immunity genes through cooperation with the FAcilitate Chromatin Transcription (FACT) complex. Furthermore, our study suggests that high MED16 expression may serve as a potential biomarker for myelodysplastic syndromes (MDS). Knockdown of MED16 in bone marrow mononuclear cells (BMMNCs) of MDS promotes erythroid differentiation, which may offer a potential therapeutic strategy for hematopoietic dysplasia diseases. Our findings demonstrate that MED16 acts as a negative regulator of erythroid and myeloid development and demonstrate its critical role in modulating the chromatin landscape in cooperation with RUNX1 and the FACT complex.
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 GSE248804_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 PRJNA1046034 and SRA study SRP474766. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
D0CD34_RUNX1 ×2 D4CD34_RUNX1 ×2 D4CD34SCR_SPT16 ×2 D4CD34SHI_SPT16 ×2 D0CD34_MED16 ×2 D4CD34_MED16 ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 12 sample titles; they account for 12 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
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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.