HNF4a controls growth, identity and response to KRAS inhibition in IMA.
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 60 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
- 60 samples: 60 samples, each with a distinct title — no replicated groupsGroups 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 GSE294573_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 PRJNA1250508 and SRA study SRP578440. Searching any of these in the dataset finder brings you back here.
Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.
How we read this: Read from 60 sample titles: 60 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.
- GSM8911530 19825X1_1311G#4_KNH_rep1
- GSM8911531 19825X2_1311G#4_KNH_rep2
- GSM8911532 19825X3_1311G#4_KN_rep1
- GSM8911533 19825X4_1311G#4_KN_rep2
- GSM8911534 23772X1_KN_GEMM_rep1
- GSM8911535 23772X2_KN_GEMM_rep2
- GSM8911536 23772X3_KN_GEMM_rep3
- GSM8911537 23772X4_KN_GEMM_rep4
- GSM8911538 23772X5_KNH_GEMM_rep1
- GSM8911539 23772X6_KNH_GEMM_rep2
- GSM8911540 24130X1_429A_KN_rep1
- GSM8911541 24130X2_429A_KNH_rep1
- GSM8911542 24130X3_429A_KN_rep2
- GSM8911543 24130X4_429A_KNH_rep2
- GSM8911544 24139X1_KNH_GEMM_rep3
- GSM8911545 24139X2_KNH_GEMM_rep4
- GSM8911546 23784X1 KN
- GSM8911547 23784X2 KNH
- GSM8911548 20899X1_1311G#5_KN_input_rep1
- GSM8911549 20899X2_1311G#5_KNH_input_rep1
- GSM8911550 20899X3_1311G#5_KN_FOXA1_rep1
- GSM8911551 20899X4_1311G#5_KNH_FOXA1_rep1
- GSM8911552 21021X1_1311G#5_KN_FOXA1_rep2
- GSM8911553 21021X2_1311G#5_KNH_FOXA1_rep2
- GSM8911554 21021X3_1311g#5_KN_input_rep2
- GSM8911555 21021X4_1311G#5_KNH_input_rep2
- GSM8911556 23754X1_1311g#5_KN Hnf4a_rep1
- GSM8911557 23754X2_1311g#5_KN_Input_rep1
- GSM8911558 23754X3_1311g#5_KN_Hnf4a_rep2
- GSM8911559 23754X4_1311g#5_KN_input_rep2
- GSM8911560 24131X1_429A_KN_input_rep1
- GSM8911561 24131X2_429A_KN_Hnf4a_rep1
- GSM8911562 24131X3_429A_KN_input_rep2
- GSM8911563 24131X4_429A_KN_Hnf4a_rep2
- GSM8911564 24137X1_GEMM_KN_HED798_FOXA1_rep1
- GSM8911565 24137X2_GEMM_KN_HED798_Hnf4a_rep1
- GSM8911566 24137X3_GEMM_KN_HED798_input_rep1
- GSM8911567 24515X1_GEMM_KN_HED934_input
- GSM8911568 24515X2_GEMM_KN_HED934_FOXA1_rep2
- GSM8911569 24515X3_GEMM_KN_HED934_FOXA2_rep1
+ 20 more — browse all 60 samples with per-sample file links →
- GSE63782 Transcriptional plasticity promotes primary and acquired resistance to BET bromodomain inhibition 103 samples shares ima, inhibition
- GSE269985 Mechanisms of resistance to oncogenic KRAS inhibition in pancreatic cancer 30 samples shares kras, inhibition
- GSE271300 A classical epithelial state drives acute resistance to KRAS inhibition in pancreas cancer 16 samples shares kras, inhibition
- GSE316054 Targeting the ADAR1 p150 isoform triggers tumor growth inhibition and antitumor immunity to overcome immunotherapy resistance 52 samples shares inhibition, growth
- GSE252773 Pharmacological inhibition of SIRT1 limits the growth of ovarian granulosa cell tumors in vitro and in preclinical mouse models 18 samples shares inhibition, growth
- GSE248948 Spatiotemporal control of SMARCA5 by a MAPK-RUNX1 axis distinguishes mutant KRAS-driven pancreatic malignancy from tissue regeneration 170 samples shares kras
- GSE272831 Adipogenesis, lipolysis, and extracellular matrix remodeling are early modulated by a triterpene-enriched natural extract in a mouse cell line and primary human adipocytes 40 samples shares ima
- GSE269664 Heterobifunctional proteomimetic polymers for targeted degradation of MYC and KRAS 33 samples shares kras
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.