Molecular Mechanisms of the MLL4 Complex in H3K4 Methylation and p53-Dependent Transcription Activation [ChIP-Seq]
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 20 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
- 20 samples: 6 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.
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 GSE308469_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 PRJNA1330720 and SRA study SRP621857. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 12 samples.
How we read this: 6 replicated groups read from 20 sample titles; they account for 12 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.
- GSM9246356 H3K4me1_MLL4WT
- GSM9246357 H3K4me1_MLL4KO
- GSM9246358 H3K4me3_MLL4WT_rep1 H3K4me3_MLL4WT
- GSM9246359 H3K4me3_MLL4KO_rep1 H3K4me3_MLL4KO
- GSM9246360 H3K27ac_MLL4WT_rep1 H3K27ac_MLL4WT
- GSM9246361 H3K27ac_MLL4KO_rep1 H3K27ac_MLL4KO
- GSM9246362 MLL4_MLL4WT
- GSM9246363 MLL4_MLL4KO
- GSM9246364 p53_MLL4WT_rep1 p53_MLL4WT
- GSM9246365 p53_MLL4KO_rep1 p53_MLL4KO
- GSM9246366 H3K4me3_MLL4WT_rep2 H3K4me3_MLL4WT
- GSM9246367 H3K4me3_MLL4KO_rep2 H3K4me3_MLL4KO
- GSM9246368 MLL1_MLL4WT
- GSM9246369 MLL1_MLL4KO
- GSM9246370 Input_MLL4WT
- GSM9246371 Input_MLL4KO
- GSM9246372 p53_MLL4WT_rep2 p53_MLL4WT
- GSM9246373 p53_MLL4KO_rep2 p53_MLL4KO
- GSM9246374 H3K27ac_MLL4WT_rep2 H3K27ac_MLL4WT
- GSM9246375 H3K27ac_MLL4KO_rep2 H3K27ac_MLL4KO
- GSE280574 mChIP-seq for high-throughput epigenomic profiling reveals a decoupling of H2A.Z and H3K4me3 in cancer 576 samples shares h3k4, chip-seq
- GSE254366 Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. 36 samples shares h3k4, methylation
- GSE284519 TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination [ChIP-seq] 93 samples shares transcription, chip-seq
- GSE296190 Hypoxic regulation of chromatin and gene transcription [ChIP-seq] 84 samples shares transcription, chip-seq
- GSE335058 Evolutionary guided transcription factor design programs novel T cell states [ChIP-Seq] 66 samples shares transcription, chip-seq
- GSE293334 Allelic topological centering by transcription factors drives oncogenic multi-enhancer transcriptional regulation [ChIP-seq] 60 samples shares transcription, chip-seq
- GSE296831 Epigenetic Context Defines the Transcriptional Activity of Canonical and Noncanonical NF-kappaB Signaling in Pancreatic Cancer [ChIP-Seq] 48 samples shares transcription, chip-seq
- GSE267597 AP-1 Mediates Oncogenic Transcription and Predicts Fatality in Lung Squamous Cell Carcinoma Patients [ChIP-seq] 36 samples shares transcription, chip-seq
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.