Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ATAC-seq of sotorasib-resistant H23 and H358 cells treated with TEAD inhibitor GNE-7883

ABSTRACT: ATAC-seq of sotorasib-resistant H23 and H358 cells treated with TEAD inhibitor GNE-7883

PROVIDER: PRJNA952671 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

ATAC-seq of sotorasib-resistant H23 and H358 cells treated with TEAD inhibitor GNE-7883

Project description:ATAC-seq of sotorasib-resistant H23 and H358 cells treated with TEAD inhibitor GNE-7883

2023-04-26 | GSE229068 | GEO

Acute and Long-Term/Resistant Gene Expression Changes in H23 Cells Due to Sotorasib Treatment

Project description:To better understand the mechanism of acquired resistance to sostorasib, we selected the H23 cells to develop an isogenic sotorasib resistant cell line. H23 cells were treated for a period of 45 days with increasing concentrations of sotorasib until the develo resistance to sostorasib.

2023-01-06 | GSE192619 | GEO

ATAC-seq of H226 cells treated with TEAD inhibitor GNE-7883

Project description:ATAC-seq of H226 cells treated with TEAD inhibitor GNE-7884

2023-04-26 | GSE229064 | GEO

RNA-seq of HCC1576 and OVCAR8 cells treated with TEAD inhibitor GNE-7883

Project description:RNA-seq of HCC1576 and OVCAR8 cells treated with TEAD inhibitor GNE-7883

2023-04-26 | GSE229066 | GEO

An allosteric pan-TEAD inhibitor blocks oncogenic YAP/TAZ signaling and overcomes KRAS G12C inhibitor resistance

Project description:The Hippo pathway is a key growth-control pathway conserved across species. The downstream effectors of the Hippo pathway YAP/TAZ are frequently activated in cancer cells by a diverse array of mechanisms to drive proliferation and survival. Based on the premise that sustained interactions between YAP/TAZ and TEADs are central to their transcriptional activities, we discovered a potent small molecule inhibitor (SMI) GNE-7883 that allosterically blocks the interactions between YAP/TAZ and all four TEAD paralogs in human cells through binding to the TEAD lipid pocket. GNE-7883 effectively reduces chromatin accessibility specifically at TEAD motifs, suppresses cell proliferation in a variety of cell line models, and achieved strong anti-tumor efficacy in vivo. Furthermore, we uncovered that GNE-7883 effectively overcomes resistance to the recently approved KRAS G12C inhibitor sotorasib in both treatment-refractory and acquired resistance cell line models, providing strong proof-of-concept of TEAD SMIs in targeting YAP/TAZ-mediated KRAS inhibitor resistance. Taken together, this work demonstrates activities of TEAD SMIs in YAP/TAZ-dependent cancers and highlights their potential broad applications in precision oncology and therapy resistance.

2023-04-26 | GSE229071 | GEO

ATAC-seq of H226 cells treated with TEAD inhibitor GNE-7883

Project description:ATAC-seq of H226 cells treated with TEAD inhibitor GNE-7883

| PRJNA952669 | ENA

Genetic changes of sotorasib-resistant cells

Project description:Sotorasib-resistant cells were established by exporsure of LU65 and MiaPACA-2 cells to increasing dose of sotorasib, up to 5 micromole. Exome sequencing was done to study the genetic changes.

2023-01-01 | E-MTAB-12144 | biostudies-arrayexpress

Acute and Long-Term/Resistant Gene Expression Changes in H23 Cells Due to Sotorasib Treatment

Project description:Acute and Long-Term/Resistant Gene Expression Changes in H23 Cells Due to Sotorasib Treatment

| PRJNA792406 | ENA

RNA-seq of HCC1576 and OVCAR8 cells treated with TEAD inhibitor GNE-7883

Project description:RNA-seq of HCC1576 and OVCAR8 cells treated with TEAD inhibitor GNE-7883

| PRJNA952668 | ENA

UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing

Project description:Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus. Pancreatic cancer cells Capan-1. Three GNE-silencing samples and three control samples.

2010-08-01 | E-GEOD-22336 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data