The functional antagonism between SIRT2 and MOF regulates cell cycle progression and genome stability [ChIP-seq]
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 24 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
- 24 samples: 8 conditions, mostly in triplicateGroups 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
- SIRT2 antagonizes MOF function during mitotic entryScience advances · 2026
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 GSE277367_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 PRJNA1162051 and SRA study SRP533137. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 24 samples.
How we read this: 8 replicated groups read from 24 sample titles; they account for 24 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.
- GSM8521127 HeLa_WT_H4K20Me1_Rep1 HeLa_WT_H4K20Me1
- GSM8521128 HeLa_WT_H4K20Me1_Rep2 HeLa_WT_H4K20Me1
- GSM8521129 HeLa_WT_H4K20Me1_Rep3 HeLa_WT_H4K20Me1
- GSM8521130 HeLa_Kmut_H4K20Me1_Rep1 HeLa_Kmut_H4K20Me1
- GSM8521131 HeLa_Kmut_H4K20Me1_Rep2 HeLa_Kmut_H4K20Me1
- GSM8521132 HeLa_Kmut_H4K20Me1_Rep3 HeLa_Kmut_H4K20Me1
- GSM8521133 HeLa_WT_INPUT_Rep1 HeLa_WT_INPUT
- GSM8521134 HeLa_WT_INPUT_Rep2 HeLa_WT_INPUT
- GSM8521135 HeLa_WT_INPUT_Rep3 HeLa_WT_INPUT
- GSM8521136 HeLa_Kmut_INPUT_Rep1 HeLa_Kmut_INPUT
- GSM8521137 HeLa_Kmut_INPUT_Rep2 HeLa_Kmut_INPUT
- GSM8521138 HeLa_Kmut_INPUT_Rep3 HeLa_Kmut_INPUT
- GSM8521139 MEFs_WT_H4K20Me1_Rep1 MEFs_WT_H4K20Me1
- GSM8521140 MEFs_WT_H4K20Me1_Rep2 MEFs_WT_H4K20Me1
- GSM8521141 MEFs_WT_H4K20Me1_Rep3 MEFs_WT_H4K20Me1
- GSM8521142 MEFs_MOFKO_H4K20Me1_Rep1 MEFs_MOFKO_H4K20Me1
- GSM8521143 MEFs_MOFKO_H4K20Me1_Rep2 MEFs_MOFKO_H4K20Me1
- GSM8521144 MEFs_MOFKO_H4K20Me1_Rep3 MEFs_MOFKO_H4K20Me1
- GSM8521145 MEFs_WT_INPUT_Rep1 MEFs_WT_INPUT
- GSM8521146 MEFs_WT_INPUT_Rep2 MEFs_WT_INPUT
- GSM8521147 MEFs_WT_INPUT_Rep3 MEFs_WT_INPUT
- GSM8521148 MEFs_MOFKO_INPUT_Rep1 MEFs_MOFKO_INPUT
- GSM8521149 MEFs_MOFKO_INPUT_Rep2 MEFs_MOFKO_INPUT
- GSM8521150 MEFs_MOFKO_INPUT_Rep3 MEFs_MOFKO_INPUT
- GSE245731 HNF4G and FOXA1 are context-specific drivers of pancreatic cancer progression [ChIP-seq] 172 samples shares progression, chip-seq
- GSE260742 DOT1L provides transcriptional memory through PRC1.1 antagonism [ChIP-Seq] 158 samples shares antagonism, chip-seq
- GSE99284 Enhancer reprogramming promotes pancreatic cancer progression and metastasis [ChIP-seq] 90 samples shares progression, chip-seq
- GSE245734 HNF4G and FOXA1 are context-specific drivers of pancreatic cancer progression 225 samples shares progression
- GSE263043 Combined antagonism of Interleukin 6 and Oncostatin M provide both anti-inflammatory and anti-fibrotic benefit in pulmonary fibrosis 171 samples shares antagonism
- GSE298580 Dual inhibition of FACT and RRM2 suppresses the progression of pancreatic ductal adenocarcinoma driven by the oncohistone H2BG53D 64 samples shares progression
- GSE333317 Adrenal-derived factors drive progression of sclerotic prostate cancer in bone 48 samples shares progression
- GSE245733 HNF4G and FOXA1 are context-specific drivers of pancreatic cancer progression [RNA-seq] 29 samples shares progression
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.