Elucidating the role of DEAF1 in neurodevelopment and shared molecular pathways in high-risk autism genes using cortical organoids
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 11 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
- 11 samples: 11 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.
Read the full summary ↓
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.
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.
Supplementary files
The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE304228_RAW.tar (it can run to tens of gigabytes).
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 PRJNA1299431 and SRA study SRP605593. Searching any of these in the dataset finder brings you back here.
Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.
How we read this: Read from 11 sample titles: 11 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.
- GSM9145486 CNTL-1, D70 (RNA-Seq)
- GSM9145487 CNTL-2, D70 (RNA-Seq)
- GSM9145488 CNTL-3, D70 (RNA-Seq)
- GSM9145489 MUT-1, D70 (RNA-Seq)
- GSM9145490 MUT-2, D70 (RNA-Seq)
- GSM9145491 MUT-3, D70 (RNA-Seq)
- GSM9145492 H1 (ATAC-seq)
- GSM9145493 CNTL (ATAC-seq)
- GSM9145494 MUT (ATAC-seq)
- GSM9145495 Input (ChIP-Seq)
- GSM9145496 DEAF1 (ChIP-Seq)
- GSE289912 APOE4 impacts cortical neurodevelopment and alters network formation in human brain organoids 32 samples shares neurodevelopment, organoids, cortical
- GSE231321 Phosphorylation of 53BP1 by ATM enforce neurodevelopmental programs in cortical organoids 30 samples shares neurodevelopment, organoids, cortical
- GSE328362 Cortical organoids reveal human-specific role of METTL5 in neurodevelopment via regulation of CHCHD2 12 samples shares neurodevelopment, organoids, cortical
- GSE334981 Cortical organoids reveal human-specific role of METTL5 in neurodevelopment via regulation of CHCHD2 [scRNA-seq] 6 samples shares neurodevelopment, organoids, cortical
- GSE119316 Impaired oxysterol-liver X receptor signaling underlies aberrant cortical neurogenesis in a stem cell model of neurodevelopmental disorder 71 samples shares neurodevelopment, cortical
- GSE249942 Requirements for the neurodevelopmental disorder-associated gene ZNF292 in human cortical interneuron development and function 55 samples shares neurodevelopment, cortical
- GSE233916 Mutant Huntingtin impairs neurodevelopment in human brain organoids through CHCHD2-mediated neurometabolic failure 36 samples shares neurodevelopment, organoids
- GSE240337 Elucidating the molecular pathology of DEPDC5 mutation induced mTOR-hyperactivation associated with epilepsy and autism spectrum disorder 36 samples shares elucidating, autism
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.