Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

ABSTRACT: MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE126143 | GEO | 2019/12/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

Project description:Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

| PRJNA521147 | ENA

RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

Project description:In this study we identified genes regulated by CASZ1b in SMS-CTR cells

2019-12-26 | GSE126145 | GEO

Investigate the affect of CASZ1b on chromatin accessibility in SMS-CTR cells

Project description:In SMS-CTR cells, the overexpression of CASZ1b in SMS-CTR cells led to a modification of regional chromation accessibility.

2019-12-26 | GSE126140 | GEO

RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

Project description:RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

| PRJNA521143 | ENA

Genome-wide mapping of CASZ1b binding sites and investigate its effect on chromatin status in SMS-CTR cells [CTRtetCASZ1b]

Project description:In SMS-CTR cells, we identified genomewide binding sites of CASZ1b. The overexpression of CASZ1b in SMS-CTR cells led to a regional epigenetic modification.

2019-12-26 | GSE126142 | GEO

Investigate the affect of CASZ1b on chromatin accessibility in SMS-CTR cells

Project description:Investigate the affect of CASZ1b on chromatin accessibility in SMS-CTR cells

| PRJNA521144 | ENA

Efficacy of trametinib and dabrafenib associated with radioactive iodine for the treatment of refractory metastatic differentiated thyroid cancer

Project description:Efficacy of a selective MEK (trametinib) and BRAFV600E (dabrafenib) inhibitors associated with radioactive iodine (RAI) for the treatment of refractory metastatic differentiated thyroid cancer with RAS or BRAFV600E mutation. To evaluate the objective response rate according to RECIST criteria in thyroid cancer patients with metastatic radioactive iodine (RAI) refractory disease, 6 months after a treatment combining in each arm of the phase II trial (patients with RAS mutation or patients with BRAFV600E mutation): - Arm A: 6 weeks of trametinib followed by RAI treatment (5.5 GBq following rhTSH) in patients with RAS mutation - Arm B: 6 weeks of trametinib plus dabrafenib followed by RAI treatment (5.5 GBq following rhTSH) in patients with BRAFV600E mutation

2023-09-01 | E-MTAB-12837 | biostudies-arrayexpress

Efficacy of trametinib and dabrafenib associated with radioactive iodine for the treatment of refractory metastatic differentiated thyroid cancer (KRAS cohort)

Project description:Efficacy of a selective MEK (trametinib) and BRAFV600E (dabrafenib) inhibitors associated with radioactive iodine (RAI) for the treatment of refractory metastatic differentiated thyroid cancer with RAS (current cohort) or BRAFV600E mutation. To evaluate the objective response rate according to RECIST criteria in thyroid cancer patients with metastatic radioactive iodine (RAI) refractory disease, 6 months after a treatment combining in each arm of the phase II trial (patients with RAS mutation or patients with BRAFV600E mutation): - Arm A: 6 weeks of trametinib followed by RAI treatment (5.5 GBq following rhTSH) in patients with RAS mutation - Arm B: 6 weeks of trametinib plus dabrafenib followed by RAI treatment (5.5 GBq following rhTSH) in patients with BRAFV600E mutation

2023-09-01 | E-MTAB-12900 | biostudies-arrayexpress

CASZ1 is essential for activation of epidermal terminal differentiation

Project description:CASZ1 is a novel and potent activator of terminal epidermal differentiation. CASZ1 knockdown inhibits transcription of the epidermal differentiation program. p63 and p300 are required to activate CASZ1 expression.

2024-02-26 | GSE241873 | GEO

Capicua-dependent transcriptional changes in human cancer cell lines treated with trametinib

Project description:We performed a genome-scale CRISPR screen in a KRAS-mutant pancreatic cancer cell line treated with the MEK inhibitor trametinib, and found that loss of the transcriptional repressor CIC confers resistance to MEK inhibition. We determined that CIC loss also confers resistance to MEK or BRAF inhibition in lung cancer, colorectal cancer, and melanoma cell lines with mutant RAS or BRAF. CIC is a transcriptional repressor that is phosphorylated and inhibited by the MAPK pathway. We hypothesized that inhibition of the MAPK pathway would lead to activation of CIC and repression of CIC target genes. Loss of CIC would therefore restore expression of these genes, conferring drug resistance. To identify the relevant CIC target genes that mediate trametinib resistace, we generated 4 Cas9-expressing cell lines from different lineages and with different RAS or RAF mutations, and generated control (gGFP) or CIC-knockout (gCIC) cell lines. We treated cells with DMSO or trametinib for 24 hours, and performed NRA-seq. We found that trametinib treatment reduces expression of at least one member of the PEA3 family of ETS transcription factors (ETV1, ETV4, and ETV5) in all cell lines assessed, and that loss of CIC results in maintained expression of these genes despite MEK inhibition. We further validated that ETV1, 4, and 5 expression was necessary for resistance mediated by CIC loss; and that ETV1, 4, or 5 expression was sufficient to confer trametinib resistance.

2017-05-31 | GSE78519 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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