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The catalytically inactive KDM5B-NTT isoform associates with chromatin and increases H3K4 trimethylation in breast cancer cells

GSE341885 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 13 samples Submitted 2026/07/31 Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 13 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
Breast cancerThis series is part of our curated briefing on it.
Samples
13 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)
Background. Histone lysine demethylases are key regulators of cancer-related processes. Beyond their enzymatic activity, catalytically independent functions are increasingly recognized. We previously identified a N-terminal truncated and catalytically inactive isoform of KDM5B, called NTT, stably expressed in several human cell lines.
Read the full summary ↓
Overex-pression of NTT-FLAG in MCF7 breast cancer cells was shown to increase global H3K4me3 levels and modulate transcription of several genes. Methods. In this study, we used the CUT&RUN assay to investigate the genomic lo-calization and the local effects on histone methylation of ectopically expressed NTT-FLAG. Moreover, phenotypic assays were performed to assess the effects of NTT-FLAG over-expression on cell migration and invasion. Results. NTT-FLAG preferentially associates with actively transcribed genes enriched in H3K4me3 at promoter regions, contributing to increased H3K4me3 levels at target sites. Functionally, NTT overexpression enhances MCF7 cell migration and invasiveness. Conclusions. Our findings support a model in which NTT and PLU-1 scan chromatin via PHD1 in a transient, low-affinity manner, while H3K4me3 stabilizes their binding by interacting with PHD3. However, catalytic activity likely depends on corepressor en-gagement, whose availability is influenced by endogenous KDM5B levels. Functionally, NTT appears to enhance cell migration and invasiveness by regulating genes such as PLAUR and CSF1, supporting its role in driving tumour-associated phenotypes inde-pendently of catalytic activity.
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 GSE341885_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 PRJNA1504432 and SRA study SRP722554. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
MCF7, Empty-Flag, H3K4me3, ×2 MCF7, NTT-Flag, H3K4me3, ×2 MCF7, PLU1-Flag, H3K4me3, ×2 MCF7, Empty-Flag, ×2 MCF7, NTT-Flag, ×2 MCF7, PLU1-Flag, ×2 MCF7, NTT-Flag, IgG ×1

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 13 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
More Breast cancer datasets

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