Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequencing of Naive CD8 T cells isolated from Brca1 wildtype and Brca1 het splenocytes

ABSTRACT: To determine the impact of Brca1 gene heterozygosity on transcriptomics of CD8+ T cells, we carried out bulk RNA-sequencing (RNA-seq) using naive CD8+ T cells isolated from WT and Het mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE191217 | GEO | 2024/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA sequencing of Naive CD8 T cells isolated from Brca1 wildtype and Brca1 het splenocytes

Project description:RNA sequencing of Naive CD8 T cells isolated from Brca1 wildtype and Brca1 het splenocytes

| PRJNA790617 | ENA

Heterozygous BRCA1 Deletion, but not Complete BRCA1 Loss, Confers Resistance to Androgen Deprivation Therapy in Prostate Cancer

Project description:BRCA1 is biallelically deleted or mutated in at least 1.9% of prostate tumors, but whether BRCA1 deficiency influences resistance to androgen deprivation therapy (ADT) and prostate cancer development remains elusive. Here we surprisingly find that in human, BRCA1 heterozygous deletion is observed in approximately 13% of human prostate cancers, is more prevalent in neuroendocrine prostate tumors and predicts worse survival than BRCA1 homozygous deletion. In mice, we show that Brca1 heterozygosity (HET) but not Brca1 full inactivation (KO) accelerates early tumor development, invasion and resistance to ADT in Pten-null prostate tumors. Furthermore, pre-malignant tumors and organoids derived from Brca1 HET mice undergo neuroendocrine differentiation and exhibit elevated levels of the unfolded protein response potentially as a pro-survival mechanism, but not those of Brca1 KO. Our findings thus provide important insights into clinical management of prostate cancer patients, suggesting that patients heterozygous for Brca1 are prone to developing resistance to ADT and should be treated differently from patients with complete Brca1 loss.

2024-02-01 | GSE176280 | GEO

The transcriptional profilling of the thermosensitive self-incompatible het-R het-V strain undergoing cell death by incompatibility

Project description:In the filamentous fungus Podospora anserina, cell death by incompatibility can be monitored using the conditional self-incompatible (SI) het-R het-V strain. SI strains are homokaryotic strains bearing incompatible het genes in all nuclei. The co-expression of these het genes triggers cell death in all the cells and hence in the entire mycelium. The het-R het-V SI strain, bearing the two incompatible het-R and het-V genes, proved particularly convenient as cell death triggering is thermosensitive (J. Labarère et al., 1973, C R Acad Sci Hebd Seances Acad Sci D, 276) and is induced by a simple shift in growth temperature (from 32°C to 26°C).The development of this cell death reaction has been recorded for 4 h after transfer to the restrictive temperature. A time course (T0h to T4h) of the transcriptomic response to the temperature shift has been explored in parallel within SI (het-R het-V) and wild type (compatible het-r hetV) s strains.

2013-01-01 | GSE21659 | GEO

The transcriptional profilling of the thermosensitive self-incompatible het-R het-V strain undergoing cell death by incompatibility

Project description:In the filamentous fungus Podospora anserina, cell death by incompatibility can be monitored using the conditional self-incompatible (SI) het-R het-V strain. SI strains are homokaryotic strains bearing incompatible het genes in all nuclei. The co-expression of these het genes triggers cell death in all the cells and hence in the entire mycelium. The het-R het-V SI strain, bearing the two incompatible het-R and het-V genes, proved particularly convenient as cell death triggering is thermosensitive (J. LabarM-CM-(re et al., 1973, C R Acad Sci Hebd Seances Acad Sci D, 276) and is induced by a simple shift in growth temperature (from 32M-BM-0C to 26M-BM-0C).The development of this cell death reaction has been recorded for 4 h after transfer to the restrictive temperature. A time course (T0h to T4h) of the transcriptomic response to the temperature shift has been explored in parallel within SI (het-R het-V) and wild type (compatible het-r hetV) s strains. With Platform GPL10116 : reference design with 2 strains: a WT strain and het-R het-V self-incompatible strain (J. LabarM-CM-(re et al., 1973, C R Acad Sci Hebd Seances Acad Sci D, 276). Each strain with four biological replicates; the common reference is a pool of four conditions M48h, M96h, C48h and C96h ; Conditions are labelled in Cy3 and the common reference in Cy5.

2013-01-01 | E-GEOD-21659 | biostudies-arrayexpress

Genomic profiling of Estrogen receptor positive BRCA1-mutated breast cancer [Nimblegen human 135K]

Project description:Purpose: As estrogen receptor (ER)-positive breast cancer in BRCA1 mutation carriers arises at an older age with less aggressive tumor characteristics than ER negative BRCA1 mutated breast cancer, it has been suggested that these tumors are ?sporadic? and not BRCA1-driven. With the introduction of targeted treatments specific for tumors with a non-functioning BRCA1 or BRCA2 gene, the question whether the BRCA genes are impaired in the tumor, is highly relevant. Therefore, we performed genomic profiling of BRCA1-mutated ER+ tumors. Experimental design: Genomic profiling, BRCA1 promoter methylation assessment, and loss of heterozygosity analysis were done on 16 BRCA1-mutated ER+ tumors. Results were compared with 57 BRCA1-mutated ER- tumors, 36 BRCA2-mutated ER+ associated tumors, and 182 sporadic ER+ tumors [GSE9021, GSE9114, GSE16511, GSE50407] Results: The genomic profile of BRCA1-mutated ER+ tumors was different from BRCA1-mutated ER- breast tumors, but highly similar to BRCA2-mutated ER+ tumors. In 83% of the BRCA1-mutated ER+ tumors, loss of the wildtype BRCA1 allele was observed. In addition, clinico-pathological variables in BRCA1-mutated ER+ cancer were also more similar to BRCA2-mutated ER+ and sporadic ER+ breast cancer than to BRCA1 mutated ER- cancers. Conclusions: As BRCA1-mutated ER+ tumors show a BRCAness copy number profile and LOH, it is likely that the loss of a functional BRCA1 protein plays a role in tumorigenesis in BRCA1-mutated ER+ tumors. Therefore, we hypothesize that these tumors are sensitive to drugs targeting the BRCA1 gene defect, providing new targeted treatment modalities for advanced BRCA-deficient, ER-positive breast cancer.

2016-10-01 | GSE77603 | GEO

Genomic profiling of Estrogen receptor positive BRCA1-mutated breast cancer [human 3.5k BAC array]

Project description:Purpose: As estrogen receptor (ER)-positive breast cancer in BRCA1 mutation carriers arises at an older age with less aggressive tumor characteristics than ER negative BRCA1 mutated breast cancer, it has been suggested that these tumors are ?sporadic? and not BRCA1-driven. With the introduction of targeted treatments specific for tumors with a non-functioning BRCA1 or BRCA2 gene, the question whether the BRCA genes are impaired in the tumor, is highly relevant. Therefore, we performed genomic profiling of BRCA1-mutated ER+ tumors. Experimental design: Genomic profiling, BRCA1 promoter methylation assessment, and loss of heterozygosity analysis were done on 16 BRCA1-mutated ER+ tumors. Results were compared with 57 BRCA1-mutated ER- tumors, 36 BRCA2-mutated ER+ associated tumors, and 182 sporadic ER+ tumors [GSE9021, GSE9114, GSE16511, GSE50407]. Results: The genomic profile of BRCA1-mutated ER+ tumors was different from BRCA1-mutated ER- breast tumors, but highly similar to BRCA2-mutated ER+ tumors. In 83% of the BRCA1-mutated ER+ tumors, loss of the wildtype BRCA1 allele was observed. In addition, clinico-pathological variables in BRCA1-mutated ER+ cancer were also more similar to BRCA2-mutated ER+ and sporadic ER+ breast cancer than to BRCA1 mutated ER- cancers. Conclusions: As BRCA1-mutated ER+ tumors show a BRCAness copy number profile and LOH, it is likely that the loss of a functional BRCA1 protein plays a role in tumorigenesis in BRCA1-mutated ER+ tumors. Therefore, we hypothesize that these tumors are sensitive to drugs targeting the BRCA1 gene defect, providing new targeted treatment modalities for advanced BRCA-deficient, ER-positive breast cancer.

2016-10-01 | GSE77604 | GEO

Transcriptomic profile of germinal center B cells from conditional GC-specific (Cg1-Cre) Crebbp-HET, Kmt2d-HET, and compound Crebbp-HET/Kmt2d-HET mice, with littermate controls

Project description:Transcriptomic profile of germinal center B cells from conditional GC-specific (Cg1-Cre) Crebbp-HET, Kmt2d-HET, and compound Crebbp-HET/Kmt2d-HET mice, with littermate controls

| PRJNA909299 | ENA

Spatial-temporal tracking of Brca1-driven breast tumorigenesis from sporadic mutant cells with a genetic mosaic mouse model

Project description:We utilized a genetic tool termed Mosaic Analysis with Double Markers (MADM) to achieve a sporadic loss of heterozygosity of Brca1 & Trp53 in mouse mammary epithelial cells and concomitantly label them with GFP. This MADM-based mouse model initiated cancer with sparse GFP+ mutant cells and developed mammary tumors that resemble human disease at pathological, transcriptomic, and genomic levels. This dataset provides bulk RNA sequencing of twelve mammary tumors from MADM Brca1-Trp53 animals.

2023-10-16 | GSE214433 | GEO

Next Generation Sequencing Analysis of chemically reprogrammed osteoblasts from Beta-actin Wildtype (WT) Heterozygotes (HET) and knockout (KO) Mouse Embryonic Fibroblast (MEFs)

Project description:mRNA profiles of chemically reprogrammed osteoblasts from Beta-actin Wildtype (WT) Heterozygotes (HET) and knockout (KO) Mouse Embryonic Fibroblast (MEFs)

2019-08-06 | GSE135392 | GEO

Na,K-ATPase alpha 1 het. heart

Project description:Whole hearts from wild-type and Na,K-ATPase alpha 1 het. mice. Adult male, 8-16 weeks old on a 129/BSwiss background. Keywords: repeat sample

2004-11-19 | GSE1134 | GEO

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