Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [cell lines]

ABSTRACT: To investigate the mechanism underlying the effect of Brn2-loss we extracted mRNA from Braf-Pten-Brn2-wt, Braf-Pten-Brn2-het, and Braf-Pten-Brn2-hom mouse melanomas and performed microarray-based transcriptome analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE163085 | GEO | 2021/04/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [tumors]

Project description:To investigate the mechanism underlying the effect of Brn2-loss we extracted mRNA from Braf-Pten-Brn2-wt, Braf-Pten-Brn2-het, and Braf-Pten-Brn2-hom mouse melanomas and performed microarray-based transcriptome analysis.

2021-04-13 | GSE126524 | GEO

Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2

Project description:Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2

| PRJNA684750 | ENA

Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [tumors]

Project description:Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [tumors]

| PRJNA522269 | ENA

Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [cell lines]

Project description:Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [cell lines]

| PRJNA684751 | ENA

Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-04-13 | GSE163086 | GEO

BRN2 expression increases anoikis resistance in melanoma.

Project description:Melanoma tumors are highly heterogeneous, comprising of many cell populations that vary in their potential for growth and invasion. Differential transcription factor expression contributes to these phenotypic traits. BRN2, a member of the POU domain family of transcription factors is thought to play important roles in melanoma invasion and metastasis. However, how BRN2 functions during the metastatic process of melanoma remains largely unknown. We therefore investigated the effects of BRN2 expression in melanoma cells with no or low constitutive expression using a doxycycline-inducible system. Induction of BRN2 expression led to reduced proliferation and partial resistance to an inhibitor of mutated BRAF. Whole genome profiling analysis revealed novel targets and signaling pathway changes related to prevention of cell death induced by detachment from the extracellular matrix, known as anoikis resistance. Further investigation confirmed increased survival of BRN2 expressing cell lines in non-adherent conditions. Functionally, expression of BRN2 promoted induction of c-MET levels as well as increased phosphorylation of STAT3. Treatment with crizotinib, a c-MET inhibitor, decreased cellular viability of BRN2 expressing cells under non-adherent conditions to death by anoikis. These results highlight the importance of a largely overlooked transcription factor in the progression and metastasis of melanoma, and may suggest a strategy to target BRN2 expressing cells resistant to therapy and cell death by anoikis.

2020-02-25 | GSE145806 | GEO

Optogenetic induction of Brn2 drive neural differentiation

Project description:We use optical induction of Brn2 to probe mechanisms for gating embryonic stem cell differentiation mRNA-seq time-course following Brn2 induciton

2015-08-26 | E-GEOD-71889 | biostudies-arrayexpress

Neratinib, a pan ERBB/HER inhibitor, restores sensitivity of PTEN-null, BRAFV600E melanoma to BRAF/MEK inhibition

Project description:Approximately 50% of melanomas harbor an activating BRAFV600E mutation. Standard of care involves a combination of inhibitors targeting mutant BRAF and MEK1/2, the substrate for BRAF in the MAPK pathway. PTEN loss of function mutations occur in 40% of BRAFV600E melanomas, resulting in increased PI3K/AKT activity that enhances resistance to BRAF/MEK combination inhibitor therapy. To compare the response of PTEN null to PTEN wild type cells in an isogenic background, CRISPR was used to knock out PTEN a melanoma cell line that harbors a BRAFV600E mutation. RNA sequencing and functional kinome analysis revealed the loss of PTEN led to an induction of FOXD3 and an increase in expression of the FOXD3 target gene, ERBB3/HER3. Inhibition of BRAF and MEK1/2 in PTEN null, BRAFV600Ecells dramatically induced expression of ERBB3/HER3 relative to wild type cells. A synergy screen of epigenetic modifiers and kinase inhibitors in combination with BRAFi/MEKi identified the pan ERBB/HER inhibitor, neratinib, as reversing the resistance observed in PTEN null, BRAFV600Ecells. The findings indicate that PTEN null BRAFV600E melanoma exhibits increased reliance on ERBB/HER signaling when treated with clinically approved BRAFi/MEKi combinations. Future studies are warranted to test neratinib reversal of resistance in patient melanomas expressing ERBB3/HER3 in combination with its dimerization partner ERBB2/HER2.

2024-04-23 | GSE255541 | GEO

ChIP-Seq of Sox2 and Brn2 in ESCs, NPCs, and differentiating ESCs

Project description:We analyzed the genome-wide binding of Sox2 and POU factor partner factors, Oct4 in ESCs (using published datasets PMID:18692474 and GSM307137, GSM307154, GSM307155) and Brn2 in NPCs. We found that Sox2 and Oct4 co-occupied a large subset of promoters and enhancers in ESCs, but that Sox2 and Brn2 co-occupy predominantly enhancers. Further, we overexpressed Brn2 in differentiating ESCs and showed that ectopic Brn2 recruited Sox2 to NPC-specific targets, resulting in skewed differentiation towards the neural lineage. Examination of transcription factor binding in ESCs, NPCs, and differentiating ESCs by ChIP-Seq.

2013-02-20 | E-GEOD-35496 | biostudies-arrayexpress

ChIP-Seq of Sox2 and Brn2 in ESCs, NPCs, and differentiating ESCs

2013-02-20 | GSE35496 | GEO