Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ATAC-Seq chromatin profiling of Suz12-deleted or wild-type organoids derived from basal or luminal mouse mammary epithelial cells

ABSTRACT: ATAC-Seq chromatin profiling of Suz12-deleted or wild-type organoids derived from basal or luminal mouse mammary epithelial cells

PROVIDER: PRJNA478459 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7451480_1.fastq.gz	Fastqsanger.gz
	SRR7451480_2.fastq.gz	Fastqsanger.gz
	SRR7451490_1.fastq.gz	Fastqsanger.gz
	SRR7451490_2.fastq.gz	Fastqsanger.gz
	SRR7451481_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

RNA-seq expression profiling of Suz12-deleted or wild-type organoids derived from basal or luminal mouse mammary epithelial cells.

Project description:Total RNA was extracted from organoids grown from single sorted luminal or basal populations from the mammary glands of Rosa26-creERT2 Suz12 flox female mice. Cultures were treated with 4-hydroxytamoxifen to induce deletion of Suz12.

2018-06-28 | GSE107626 | GEO

ATAC-Seq chromatin profiling of Suz12-deleted or wild-type organoids derived from basal or luminal mouse mammary epithelial cells

Project description:Fixed DNA was isolated from organoids grown from single sorted luminal or basal populations from the mammary glands of Rosa26-creERT2 Suz12 flox female mice. Cultures were treated with 4-hydroxytamoxifen to induce deletion of Suz12.

2018-06-28 | GSE116430 | GEO

RNA-seq expression profiling of Suz12-deleted or wild-type organoids derived from basal or luminal mouse mammary epithelial cells.

Project description:RNA-seq expression profiling of Suz12-deleted or wild-type organoids derived from basal or luminal mouse mammary epithelial cells.

| PRJNA420891 | ENA

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Project description:Basal breast cancers, an aggressive breast cancer subtype that has poor treatment options, are thought to arise from luminal mammary epithelial cells that undergo basal-like plasticity through poorly understood mechanisms. Using genetic mouse models and ex vivo primary organoid cultures, we show that conditional co-deletion of the LATS1 and LATS2 kinases, key effectors of Hippo pathway signaling, in mature mammary luminal epithelial cells promotes the development of basal-like carcinomas that metastasize over time. Genetic co-deletion experiments revealed that phenotypes resulting from the loss of LATS1/2 activity are dependent on the transcriptional regulators YAP/TAZ. Notably, transcriptional analyses of LATS1/2-deleted mammary epithelial cells revealed a gene expression program that associates with human basal breast cancers. Our study demonstrates in vivo roles for the LATS1/2 kinases in mammary epithelial homeostasis and luminal-basal fate control and implicates signaling networks induced upon the loss of LATS1/2 activity in the development of basal breast cancers.

2022-09-26 | GSE196555 | GEO

RNA-seq and ATAC-Seq profiling of Suz12-deleted or wild-type organoids derived from basal or luminal mouse mammary epithelial cells

Project description:RNA-seq and ATAC-Seq profiling of Suz12-deleted or wild-type organoids derived from basal or luminal mouse mammary epithelial cells

| PRJNA478458 | ENA

Transcriptome analysis of luminal and basal cell subpopulations in the lactating versus pregnant mammary gland

Project description:To identify genes specifically expressed in lactating mammary glands, the gene expression profiles of luminal and basal cells from different developmental stages were compared. Comparison of gene expression in luminal and basal cells harvested from the mammary glands of virgin, 18.5 day pregnant and 2 day lactating mice (2 mice per stage).

2015-01-19 | E-GEOD-60450 | biostudies-arrayexpress

RNA-seq of FACS-enriched mammary subpopulations (basal, luminal progenitor, mature luminal) from WT and ID4 knockout mice

Project description:The goal of this study was to determine the genes regulated by ID4 in mammary epithelial subpopulations. Basal, luminal progenitor, and mature luminal mammary epithelial subpopulations were FACS-sorted from adult mice that were either WT or ID4 KO in quadruplicate. RNA-seq and differential gene expression analysis was performed.

2020-05-07 | GSE149965 | GEO

Transcriptome analysis of luminal and basal cell subpopulations in the lactating versus pregnant mammary gland

2015-01-19 | GSE60450 | GEO

RNAseq of mouse mammary luminal cells

Project description:The mammary epithelia are mainly composed of two distinct lineages, the basal and luminal cells. In our MMTV-Cre; Brca1flox/flox mouse model, we found the Brca1 knockout mainly occurred in the luminal cells, which will lead the mammary tumorigenesis. To investigate the Brca1 deficiency mediated mammary tumorigenesis, we sorted the luminal cells from wild type mice and MMTV-Cre; Brca1flox/flox mice for RNAseq analysis.

2021-11-17 | GSE148613 | GEO

Rb deletion in mammary stem/progenitor epithelium induces tumors with features of luminal-B or basal-like breast cancer

Project description:The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. A subset of basal-like but none of the luminal-B tumors expressed mutant p53. These results demonstrate a causative role for Rb in the etiology of breast cancer subtypes and implicate p53 status as a determinant of tumor phenotype after Rb loss. Keywords: reference x sample Will be updated soon

2010-07-06 | E-GEOD-14457 | 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