Cooperation between the Hippo and MAPK pathway activation drives acquired resistance to TEAD inhibition
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 99 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
- 99 samples: 35 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.
- Paper
- Cooperation between the Hippo and MAPK pathway activation drives acquired resistance to TEAD inhibitionNature communications · 2025
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 GSE248208_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 PRJNA1042820 and SRA study SRP522408. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 76 samples.
How we read this: 35 replicated groups read from 99 sample titles; they account for 76 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.
- GSM7871934 Sensitive_DMSO_rep1 Sensitive_DMSO
- GSM7871935 Sensitive_DMSO_rep2 Sensitive_DMSO
- GSM7871936 Sensitive_DMSO_rep3 Sensitive_DMSO
- GSM7871937 Sensitive_GNE-7883_rep1 Sensitive_GNE-7883
- GSM7871938 Sensitive_GNE-7883_rep2 Sensitive_GNE-7883
- GSM7871939 Sensitive_GNE-7883_rep3 Sensitive_GNE-7883
- GSM7871940 Resistant_DMSO_rep1 Resistant_DMSO
- GSM7871941 Resistant_DMSO_rep2 Resistant_DMSO
- GSM7871942 Resistant_DMSO_rep3 Resistant_DMSO
- GSM7871943 Resistant_GNE-7883_rep1 Resistant_GNE-7883
- GSM7871944 Resistant_GNE-7883_rep2 Resistant_GNE-7883
- GSM7871945 Resistant_GNE-7883_rep3 Resistant_GNE-7883
- GSM7871959 H226-P_DMSO_TEAD1
- GSM7871960 H226-P_DMSO_YAP
- GSM7871961 H226-P_DMSO_FOSL1
- GSM7871962 H226-P_7883_TEAD1
- GSM7871963 H226-P_7883_YAP
- GSM7871964 H226-P_7883_FOSL1
- GSM7871965 H226-7883R_CL3_TEAD1
- GSM7871966 H226-7883R_CL3_YAP
- GSM7871967 H226-7883R_CL3_FOSL1
- GSM7871968 IgG_P_DMSO
- GSM7871969 IgG_P_7883
- GSM7871970 IgG_P7883R_CL3
- GSM7871977 shNTC_sensitive 1 shNTC_sensitive
- GSM7871978 shNTC_sensitive 2 shNTC_sensitive
- GSM7871979 shYAP+TAZ_sensitive 1 shYAP+TAZ_sensitive
- GSM7871980 shYAP+TAZ_sensitive 2 shYAP+TAZ_sensitive
- GSM7871981 shYAP+TAZ_sensitive 3 shYAP+TAZ_sensitive
- GSM7871982 304_1.1_resistant 1 304_1.1_resistant
- GSM7871983 304_1.1_resistant 2 304_1.1_resistant
- GSM7871984 304_1.1_resistant 3 304_1.1_resistant
- GSM7872303 NCI-H226 G7883 CL3
- GSM7872304 NCI-H226 DMSO (83)
- GSM7890015 NCI-H226_CL3, NCI-H226, GEX
- GSM7890016 NCI-H226_CL3, NCI-H226, ATAC
- GSM7890017 NCI-H226_CL3, NCI-H226, HTO
- GSM7890027 Sensitive_shNTC-rep1 Sensitive_shNTC
- GSM7890028 Sensitive_shNTC-rep2 Sensitive_shNTC
- GSM7890029 Sensitive_shYAP-TAZ-rep1
+ 59 more — browse all 99 samples with per-sample file links →
- GSE324062 RAS pathway activation drives clonal selection and monocytic differentiation in FLT3 and BCL2 inhibitor resistance 61 samples shares activation, resistance, drives
- GSE280280 Reprogramming of Cellular Plasticity via ETS and MYC Core-regulatory circuits During Response to MAPK Inhibition in BRAF-mutant colorectal cancer 36 samples shares mapk, inhibition
- GSE303051 Prolonged KRAS-MAPK Inhibition Induces Interferon-mediated Epithelial-to-Mesenchymal Transition and Reveals Therapeutic Opportunities. 30 samples shares mapk, inhibition
- GSE303106 Prolonged KRAS-MAPK Inhibition Induces Interferon-mediated Epithelial-to-Mesenchymal Transition and Reveals Therapeutic Opportunities [cut and run-ChipSeq] 9 samples shares mapk, inhibition
- GSE270062 Autophagy inhibition induced by EM-2 augments apoptosis via ROS-mediated ATM-Chk2-p53-p21 and MAPK pathway in lung and breast carcinoma 4 samples shares mapk, inhibition
- GSE225251 Enhancer infestation drives tumorigenic activation of inactive compartment in Epstein-Barr virus-positive nasopharyngeal carcinoma 26 samples shares activation, drives
- GSE254732 Inhibition of PCSK9 with evolocumab modulates lipoproteins and monocyte activation in high-risk ASCVD subjects 215 samples shares activation, inhibition
- GSE211434 Diverse immune suppressing cancer communications with myeloid cells prevent T cell activation and recruitment and provide resistance to cell cycle inhibitor therapy 81 samples shares activation, resistance
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.