Nuclear Factor NFAT5 Governs Cellular Plasticity-Induced KRAS-Targeted Therapy Resistance in Pancreatic Cancer
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 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
- Mus musculus (mouse)
- Samples
- 24 samples: 5 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
- NFAT5 governs cellular plasticity-driven resistance to KRAS-targeted therapy in pancreatic cancerThe Journal of experimental medicine · 2024
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 GSE252839_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 PRJNA1062800 and SRA study SRP482769. Searching any of these in the dataset finder brings you back here.
Supports a case/control comparison: 5 samples read as cases, 6 as controls.
How we read this: 5 replicated groups read from 24 sample titles; they account for 15 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.
- GSM8008714 Spontaneous tumor, 69
- GSM8008715 Spontaneous tumor, 183_Ki
- GSM8008716 Spontaneous tumor, 713_Ki
- GSM8008717 Spontaneous tumor, 752OFF
- GSM8008718 Spontaneous tumor, 756OFF
- GSM8008768 PDAC_Nfat5_kd_rep 1 PDAC_Nfat5_kd
- GSM8008769 PDAC_Nfat5_kd_rep 2 PDAC_Nfat5_kd
- GSM8008770 PDAC_Nfat5_kd_rep 3 PDAC_Nfat5_kd
- GSM8008771 PDAC_Smad3_kd_rep 1 PDAC_Smad3_kd
- GSM8008772 PDAC_Smad3_kd_rep 2 PDAC_Smad3_kd
- GSM8008773 PDAC_Smad3_kd_rep 3 PDAC_Smad3_kd
- GSM8008774 PDAC_Scramble_ctrl_rep 1 PDAC_Scramble_ctrl
- GSM8008775 PDAC_Scramble_ctrl_rep 2 PDAC_Scramble_ctrl
- GSM8008776 PDAC_Scramble_ctrl_rep 3 PDAC_Scramble_ctrl
- GSM8008777 PDAC_DMSO_rep 1 PDAC_DMSO
- GSM8008778 PDAC_DMSO_rep 2 PDAC_DMSO
- GSM8008779 PDAC_DMSO_rep 3 PDAC_DMSO
- GSM8008780 PDAC_KRN2_rep 1 PDAC_KRN2
- GSM8008781 PDAC_KRN2_rep 2 PDAC_KRN2
- GSM8008782 PDAC_KRN2_rep 3 PDAC_KRN2
- GSM8008785 PDAC_SMAD2_ChIP
- GSM8008786 PDAC_SMAD3_ChIP
- GSM8008787 PDAC_SMAD4_ChIP
- GSM8008788 PDAC_NFAT5_ChIP
- GSE254919 Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy [ATAC-seq] 12 samples shares resistance, pancreatic, cellular
- GSE218178 Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance 183 samples shares resistance, pancreatic
- GSE218173 Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance [acid] 150 samples shares resistance, pancreatic
- GSE278100 Foxa1-Mediated Chromatin Remodeling and Enhancer Reprogramming Promotes Gemcitabine Resistance in Pancreatic Cancer 54 samples shares resistance, pancreatic
- GSE319747 Lineage identity governs oncogene dependence in murine NSCLC models of KRAS inhibitor resistance 41 samples shares resistance, governs
- GSE218177 Adaptation to an acid microenvironment promotes pancreatic cancer organoid growth and drug resistance [drug] 33 samples shares resistance, pancreatic
- GSE227129 PRMT1 Promotes Epigenetic Reprogramming Associated with Acquired Chemoresistance in Pancreatic Cancer 29 samples shares resistance, pancreatic
- GSE275780 Dual Targeting of STING and PI3Kγ Eliminates Regulatory B Cells to Overcome STING Resistance for Pancreatic Cancer Immunotherapy [RNA-seq] 17 samples shares resistance, pancreatic
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.