An EZH2—SREBP2 axis promotes cholesterol biosynthesis and represents a noncanonical vulnerability in tumorigenesis
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 79 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
- 79 samples: 22 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.
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 GSE287355_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 PRJNA1212202 and SRA study SRP682868. Searching any of these in the dataset finder brings you back here.
Supports a case/control comparison: 3 samples read as cases, 18 as controls.
How we read this: 22 replicated groups read from 79 sample titles; they account for 44 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.
- GSM8366913 HepG2_shControl_1 HepG2_shControl
- GSM8366914 HepG2_shControl_2 HepG2_shControl
- GSM8366915 HepG2_shEZH2_1 HepG2_shEZH2
- GSM8366916 HepG2_shEZH2_2 HepG2_shEZH2
- GSM8366917 HepG2_shSREBP2 #664_1 HepG2_shSREBP2 #664
- GSM8366918 HepG2_shSREBP2 #664_2 HepG2_shSREBP2 #664
- GSM8366919 HepG2_shSREBP2 #665_1 HepG2_shSREBP2 #665
- GSM8366920 HepG2_shSREBP2 #665_2 HepG2_shSREBP2 #665
- GSM8366921 HepG2_shSREBP2 #667_1 HepG2_shSREBP2 #667
- GSM8366922 HepG2_shSREBP2 #667_2 HepG2_shSREBP2 #667
- GSM8366923 Huh7_shControl_1 Huh7_shControl
- GSM8366924 Huh7_shControl_2 Huh7_shControl
- GSM8366925 Huh7_shEZH2_1 Huh7_shEZH2
- GSM8366926 Huh7_shEZH2_2 Huh7_shEZH2
- GSM8366927 HepG2_DMSO_1 HepG2_DMSO
- GSM8366928 HepG2_DMSO_2 HepG2_DMSO
- GSM8366929 HepG2_MS7126_1 HepG2_MS7126
- GSM8366930 HepG2_MS7126_2 HepG2_MS7126
- GSM8366931 HepG2_C24_1 HepG2_C24
- GSM8366932 HepG2_C24_2 HepG2_C24
- GSM8366933 HepG2_MS7126N1_1 HepG2_MS7126N1
- GSM8366934 HepG2_MS7126N1_2 HepG2_MS7126N1
- GSM8366935 HepG2_MS7126N2_1 HepG2_MS7126N2
- GSM8366936 HepG2_MS7126N2_2 HepG2_MS7126N2
- GSM8366937 Huh7_DMSO_1 Huh7_DMSO
- GSM8366938 Huh7_DMSO_2 Huh7_DMSO
- GSM8366939 Huh7_MS7126_1 Huh7_MS7126
- GSM8366940 Huh7_MS7126_2 Huh7_MS7126
- GSM8366942 HepG2, EZH2, CUT&RUN, CST
- GSM8366943 HepG2, EZH2, CUT&RUN, HA
- GSM8366944 HepG2, H3K27me3, CUT&RUN, CST
- GSM8366945 HepG2, H3K27me3, CUT&RUN, abcam
- GSM8366946 HepG2, H3K27ac, CUT&RUN
- GSM8366947 HepG2, H3K4me3, CUT&RUN
- GSM8366948 HepG2, SREBP2, CUT&RUN
- GSM8366950 Huh7, EZH2, CUT&RUN, CST
- GSM8366951 Huh7, EZH2, CUT&RUN, HA
- GSM8366952 Huh7, H3K27me3, CUT&RUN, CST
- GSM8366953 Huh7, H3K27me3, CUT&RUN, abcam
- GSM8366954 Huh7, H3K27ac, CUT&RUN
+ 39 more — browse all 79 samples with per-sample file links →
- GSE86532 N-Myc induces an EZH2-mediated transcriptional program driving Neuroendocrine Prostate Cancer 38 samples shares ezh2
- GSE218717 EZH2 gain-of-function mutations distort H3K27me3 landscapes and transform transcriptional responses to PRC2 inhibition. 244 samples shares ezh2
- GSE218716 EZH2 gain-of-function mutations distort H3K27me3 landscapes and transform transcriptional responses to PRC2 inhibition [ChIP-Seq/Cut&Run-Seq] 156 samples shares ezh2
- GSE266298 Epigenetic changes by EZH2 inhibition increase translocations in B cells with high AID activity or DNA repair deficiency 130 samples shares ezh2
- GSE261746 EZH2 INHIBITION ENHANCES T CELL IMMUNOTHERAPIES BY INDUCING LYMPHOMA IMMUNOGENICITY AND IMPROVING T CELL FUNCTION 54 samples shares ezh2
- GSE291509 A conserved function of EZH2-PRC2 in the repression of primitive endoderm cell fate 43 samples shares ezh2
- GSE255548 EZH2 INHIBITION ENHANCES T CELL IMMUNOTHERAPIES BY INDUCING LYMPHOMA IMMUNOGENICITY AND IMPROVING T CELL FUNCTION (RNA-Seq) 35 samples shares ezh2
- GSE267018 RNA-seq analysis of WT, SREBP knockout and SREBP2 knockout HeLa cells and liver samples of WT and SREBP2 (F167A) knockin mice 30 samples shares srebp2
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.