SUV39H1 inhibition by Chaetocin targets stemness and oncogenic networks and synergizes with ONC201 against Diffuse intrinsic pontine gliomas
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)
- Samples
- 12 samples: 2 × DMSO vs 2 × Chaetocin vs 2 × sh-ctrl vs 2 × sh-SUV39H1Groups 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
- Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201Neuro-oncology · 2024
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 GSE225029_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 PRJNA933586 and SRA study SRP422516. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 8 samples.
How we read this: 4 replicated groups read from 12 sample titles; they account for 8 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.
- GSM7037521 DMSO-1 DMSO
- GSM7037522 DMSO-2 DMSO
- GSM7037523 Chaetocin-1 Chaetocin
- GSM7037524 Chaetocin-2 Chaetocin
- GSM7037525 sh-ctrl-1 sh-ctrl
- GSM7037526 sh-ctrl-2 sh-ctrl
- GSM7037527 sh-SUV39H1-1 sh-SUV39H1
- GSM7037528 sh-SUV39H1-2 sh-SUV39H1
- GSM7037529 SU-DIPG13, H3K9me3, CST
- GSM7037530 SU-DIPG36, H3K9me3,CST
- GSM7037531 SU-DIPG13, SUV39H1,CST
- GSM7037532 SU-DIPG36, SUV39H1,CST
- GSE185651 Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance 28 samples shares inhibition, intrinsic
- GSE285823 ATR inhibition synergizes with alkylating PI polyamide targeting MYCN by suppressing DNA repair in MYCN-amplified neuroblastoma 16 samples shares inhibition, synergizes
- GSE268982 Synthetic RIG-I agonist-mediated cancer immunotherapy synergizes with MAP-Kinase inhibition against BRAF mutated melanoma 15 samples shares inhibition, synergizes
- GSE252781 Temporal dynamics of signaling and transcription underlying early adaptation to oncogenic BRAF inhibition in melanoma 13 samples shares inhibition, oncogenic
- GSE206726 Epigenetic reprogramming of the mesenchymal state by SUV39H1/H2 [ChIP-Seq] 42 samples shares suv39h1
- GSE285122 SUV39H1/2-mediated H3K9me3 restricts TE-induced immune response in Acute Myeloid Leukemia [ChIP-Seq] 18 samples shares suv39h1
- GSE282925 DNA hypomethylation promotes UHRF1- and SUV39H1/H2-dependent crosstalk between H3K18ub and H3K9me3 to reinforce heterochromatin states [RNA-Seq] 12 samples shares suv39h1
- GSE254244 Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes 112 samples shares inhibition
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.