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Impact of c-JUN deficiency on thalamus development in mice and human neural models [ATACseq, RNAseq, CUT&Tag]

GSE260732 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 23 samples Submitted 2024/12/20 Platform GPL24676
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: 23 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.
Paper
Impact of c-JUN deficiency on thalamus development in mice and human neural modelsCell & bioscience · 2024
Summary (written by the submitters)
c-Jun is a gene expression regulator. By forming homo- or heterodimer, c-Jun binds to DNA and regulates gene transcription. c-Jun is deeply involved in embryonic development but its effect on nervous system development especially in higher mammal is unclear. In this study, we combined H1ESC derived neural progenitor cells (NPCs), cerebral organoids (COs),Thalamus Organoids(ThOs) and mouse model to study the role of c-Jun in early nervous system development.
Read the full summary ↓
c-Jun KO promoted NPCs induction and differentiation while weakened NPCs’ adhesion ability. c-Jun KO COs got more robust neural ectoderm and expanded Pax6+/Nestin+ cortex-like layer while less tight junctional core. c-Jun KO mouse embryos on E14.5 showed malformation of thalamus in diencephalon with tight junction loose and cell lose. Taken together, the consistent trend in three models implied that c-Jun deletion promoted neural differentiation while weakened the tight junctions. The thalamus/diencephalon was vulnerable to dysplasia when lose c-Jun in early mouse embryonic development.
Published in
Impact of c-JUN deficiency on thalamus development in mice and human neural models
Shi J, Chen Q, Lai J et al. · Cell & bioscience 2024 · PMID 39707500 · doi:10.1186/s13578-024-01303-8
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 GSE260732_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 PRJNA1083042 and SRA study SRP492977. Searching any of these in the dataset finder brings you back here.

Study design
23 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 23 sample titles: 23 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
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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.