Accelerated RNA polymerase II elongation drives endothelial transition and plaque vulnerability: pharmacological targeting of the super elongation complex
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 40 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
- Mus musculus (mouse)
- Samples
- 40 samples: 8 conditions, mostly with about 4 replicates eachGroups 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 GSE330230_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 PRJNA1463184 and SRA study SRP698267. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 30 samples.
How we read this: 8 replicated groups read from 40 sample titles; they account for 30 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.
- GSM9721172 Control
- GSM9721173 Control_0min
- GSM9721174 Control_10min
- GSM9721175 EndMT_DMSO EndMT_DMSO
- GSM9721176 EndMT_DMSO_0min
- GSM9721177 EndMT_DMSO_10min
- GSM9721178 EndMT_KL1 EndMT_KL
- GSM9721179 EndMT_KL1_0min
- GSM9721180 EndMT_KL1_10min
- GSM9721181 EndMT_KL2 EndMT_KL
- GSM9721182 EndMT_KL2_0min
- GSM9721183 EndMT_KL2_10min
- GSM9721270 Control_DMSO
- GSM9721271 EndMT_DMSO EndMT_DMSO
- GSM9721272 EndMT_KL1 EndMT_KL
- GSM9721273 EndMT_KL2 EndMT_KL
- GSM9721955 HFD/DMSO_preventive_n1 HFD/DMSO_preventive_n
- GSM9721956 HFD/DMSO_preventive_n2 HFD/DMSO_preventive_n
- GSM9721957 HFD/DMSO_preventive_n3 HFD/DMSO_preventive_n
- GSM9721958 HFD/DMSO_preventive_n4 HFD/DMSO_preventive_n
- GSM9721959 NormalChow_preventive_n1 NormalChow_preventive_n
- GSM9721960 NormalChow_preventive_n2 NormalChow_preventive_n
- GSM9721961 NormalChow_preventive_n3 NormalChow_preventive_n
- GSM9721962 NormalChow_preventive_n4 NormalChow_preventive_n
- GSM9721963 HFD/KL-2_preventive_n1 HFD/KL-2_preventive_n
- GSM9721964 HFD/KL-2_preventive_n2 HFD/KL-2_preventive_n
- GSM9721965 HFD/KL-2_preventive_n3 HFD/KL-2_preventive_n
- GSM9721966 NormalChow_therapeutic_n1 NormalChow_therapeutic_n
- GSM9721967 NormalChow_therapeutic_n2 NormalChow_therapeutic_n
- GSM9721968 NormalChow_therapeutic_n3 NormalChow_therapeutic_n
- GSM9721969 NormalChow_therapeutic_n4 NormalChow_therapeutic_n
- GSM9721970 HFD/DMSO_therapeutic_n1 HFD/DMSO_therapeutic_n
- GSM9721971 HFD/DMSO_therapeutic_n2 HFD/DMSO_therapeutic_n
- GSM9721972 HFD/DMSO_therapeutic_n3 HFD/DMSO_therapeutic_n
- GSM9721973 HFD/DMSO_therapeutic_n4 HFD/DMSO_therapeutic_n
- GSM9721974 HFD/KL-2_therapeutic_n1 HFD/KL-2_therapeutic_n
- GSM9721975 HFD/KL-2_therapeutic_n2 HFD/KL-2_therapeutic_n
- GSM9721976 HFD/KL-2_therapeutic_n3 HFD/KL-2_therapeutic_n
- GSM9721977 HFD/KL-2_therapeutic_n4 HFD/KL-2_therapeutic_n
- GSM9721978 HFD/KL-2_therapeutic_n5 HFD/KL-2_therapeutic_n
- GSE293412 TWIST1 drives endothelial-to-mesenchymal-transition to stabilize atherosclerotic plaques 29 samples shares endothelial, transition
- GSE156337 Onco-fetal reprogramming of endothelial cells drives immunosuppressive macrophages in Hepatocellular Carcinoma 186 samples shares endothelial
- GSE97442 Genetic and pharmacological restoration of TET2 function blocks stem cell self-renewal and progression of leukemia 80 samples shares pharmacological
- GSE291636 RBBP6 orchestrates diabetic endothelial dysfunction viadisrupting JUNB-centric chromatin topology 73 samples shares endothelial
- GSE300053 Phase separation of endothelial PML drives inflammatory macrophage infiltration during liver fibrosis 69 samples shares endothelial
- GSE303627 MYST acetyltransferases are a targetable therapeutic vulnerability in SETBP1-mutant leukemia [CUT&Run] 46 samples shares vulnerability
- GSE266956 Increased translation driven by a non-canonical EZH2 cistrome creates a synthetic vulnerability in enzalutamide-resistant prostate cancer 42 samples shares vulnerability
- GSE268567 Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability 30 samples shares vulnerability
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.