ARID1A recruits TRIM28 for the essential remodeling of heterochromatin independent of SWI/SNF [ChIP-seq]
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 16 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
- 16 samples: 16 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 GSE239728_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 PRJNA1000630 and SRA study SRP452388. 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 16 sample titles: 16 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.
- GSM7670591 HCT116_Input
- GSM7670592 HCT116_IgG
- GSM7670593 HCT116_H3K9m3
- GSM7670594 HCT116_TRIM28
- GSM7670595 HCT116_ARID1A
- GSM7670596 HCT116_CTR_input
- GSM7670597 HCT116_CTR_IgG
- GSM7670598 HCT116_CTR_ARID1A
- GSM7670599 HCT116_CTR_H3K9m3
- GSM7670600 HCT116_CTR_TRIM28
- GSM7670601 HCT116_CTR_SETDB1
- GSM7670602 HCT116_shARID1A_input
- GSM7670603 HCT116_shARID1A_IgG
- GSM7670604 HCT116_shARID1A_H3K9m3
- GSM7670605 HCT116_shARID1A_TRIM28
- GSM7670606 HCT116_shARID1A_SETDB1
- GSE262093 SWI/SNF Chromatin Remodeling Complex Orchestrates Sequential Binding of Key Transcription Factors in B Cells and Restricts Aggressive Lymphoma [human ChIP-seq] 14 samples shares swi, snf, remodeling
- GSE299672 PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers [ChIP-seq] 132 samples shares swi, snf
- GSE256316 SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity [ChIP-Seq] 121 samples shares swi, snf
- GSE270784 ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency [ChIP-seq] 107 samples shares swi, snf
- GSE180483 PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [ChIP-seq] 88 samples shares swi, snf
- GSE261988 SWI/SNF is a gatekeeper of chromatin access at enhancer networks controlling triple-negative breast cancer progression [ChIP-Seq] 79 samples shares swi, snf
- GSE215023 Targeting DCAF5 suppresses SMARCB1-mutant cancer via stabilizing SWI/SNF 58 samples shares swi, snf
- GSE328419 CBFA2T3-GLIS2 fusion-mediated mSWI/SNF chromatin remodeler disruption generates cancer-specific dependencies in AMKL [Cut & Run M-07e] 34 samples shares swi, snf
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.