The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 67 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
- 67 samples: 50 distinct titles, 8 of them repeatedGroups 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 GSE293567_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 PRJNA1245248 and SRA study SRP528661. Searching any of these in the dataset finder brings you back here.
Supports a case/control comparison: 25 samples read as cases, 3 as controls.
How we read this: Read from 67 sample titles: 50 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.
- GSM8482080 K562 cells; DMSO treated_rep1
- GSM8482081 K562 cells; IAA treated_6h_rep1
- GSM8482082 K562 cells; IAA _treated_12h_rep1
- GSM8482083 K562 cells; IAA treated_24h_rep1
- GSM8482084 HUDEP2 cells; DMSO treated_rep1
- GSM8482085 HUDEP2 cells; IAA treated_6h_rep1
- GSM8482086 HUDEP2 cells; IAA treated_12h_rep1
- GSM8482087 HUDEP2 cells; IAA treated_24h_rep1
- GSM8883058 HUDEP2 cells; DMSO treated_rep1;KMT2D;ChIP-seq
- GSM8883059 HUDEP2 cells; DMSO treated_rep2;KMT2D;ChIP-seq
- GSM8883060 HUDEP2 cells; DMSO treated_rep3;KMT2D;ChIP-seq
- GSM8883061 HUDEP2 cells; 5-Ph-IAA treated_rep1;KMT2D;ChIP-seq
- GSM8883062 HUDEP2 cells; 5-Ph-IAA treated_rep2;KMT2D;ChIP-seq
- GSM8883063 HUDEP2 cells; 5-Ph-IAA treated_rep3;KMT2D;ChIP-seq
- GSM8883064 HUDEP2 cells; DMSO_rep1_Input
- GSM8883065 HUDEP2 cells; 5-Ph-IAA_rep1_Input
- GSM8883066 HUDEP2 cells; NT_rep1;H3K4me1;ChIP-seq
- GSM8883067 HUDEP2 cells; KO_rep1;H3K4me1;ChIP-seq
- GSM8883068 HUDEP2 cells; NT_rep2;H3K4me1;ChIP-seq
- GSM8883069 HUDEP2 cells; KO_rep2;H3K4me1;ChIP-seq
- GSM8883078 HUDEP2 cells; NT_rep1;H3K27ac;ChIP-seq
- GSM8883079 HUDEP2 cells; KO_rep1;H3K27ac;ChIP-seq
- GSM8883080 HUDEP2 cells; NT_rep2;H3K27ac;ChIP-seq
- GSM8883081 HUDEP2 cells; KO_rep2;H3K27ac;ChIP-seq
- GSM8883084 HUDEP2 cells; NT_rep1;GATA1;ChIP-seq
- GSM8883085 HUDEP2 cells; KO_rep1;GATA1;ChIP-seq
- GSM8883086 HUDEP2 cells; NT_rep2;GATA1;ChIP-seq
- GSM8883087 HUDEP2 cells; KO_rep2;GATA1;ChIP-seq
- GSM8883090 HUDEP2 cells;NT_rep1_Input
- GSM8883091 HUDEP2 cells;KO_rep1_Input
- GSM8883092 HUDEP2 cells;NT_rep2_Input
- GSM8883093 HUDEP2 cells;KO_rep2_Input
- GSM9277890 K562 cells; DMSO treated_rep2
- GSM9277891 K562 cells; IAA treated_6h_rep2
- GSM9277892 K562 cells; IAA treated_12h_rep2
- GSM9277893 K562 cells; IAA treated_24h_rep2
- GSM9277894 HUDEP2 cells; DMSO treated_rep2
- GSM9277895 HUDEP2 cells; IAA treated_6h_rep2
- GSM9277896 HUDEP2 cells; IAA treated_12h_rep2
- GSM9277897 HUDEP2 cells; IAA treated_24h_rep2
+ 27 more — browse all 67 samples with per-sample file links →
- GSE275664 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers 16 samples shares kmt2d, gata1, h3k4, methyltransferase, essential, erythroid, enhancers, cofactor
- GSE319075 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers [GATA1 RNA-Seq] 9 samples shares kmt2d, gata1, h3k4, methyltransferase, essential, erythroid, enhancers, cofactor
- GSE293474 KMT2D-Mediated H3K4methylation is Essential for GATA1 Transcriptional Activation in Erythropoiesis [ChIP-seq] 24 samples shares kmt2d, gata1, h3k4, essential
- GSE296270 The Histone Methyltransferase KMT2D is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration Resistant Prostate Cancer 118 samples shares kmt2d, methyltransferase
- GSE248434 Histone H3K4ac, as a marker of active transcription start sites and enhancers, plays roles in histone eviction and RNA transcription 30 samples shares h3k4, enhancers
- GSE258789 BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (RNA-seq) 20 samples shares h3k4, methyltransferase
- GSE296115 The Histone Methyltransferase KMT2D is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration Resistant Prostate Cancer [LNCaP Bulk RNA-Seq] 16 samples shares kmt2d, methyltransferase
- GSE293079 The Histone Methyltransferase KMT2D is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration Resistant Prostate Cancer [MSKPCA3 Bulk ATAC-seq] 12 samples shares kmt2d, methyltransferase
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.