Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profiling of fetal mammary cells that express ectopic levels of Sox10

ABSTRACT: We use RNA-sequencing to generate gene expression profiles of fetal mammary cells that have been induced to overexpress Sox10. These data highlight multiple important molecular mechanisms that are altered in response to this perturbation, and offer a resource to probe the basis of the stem/progenitor and EMT-like functions that are mediated by Sox10 in mammary cells. Expression profiling of fetal mammary cells that express ectopic levels of Sox10

ORGANISM(S): Mus musculus

SUBMITTER: Christopher Dravis

PROVIDER: E-GEOD-71636 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression profiling of fetal mammary cells

Project description:We use RNA-sequencing to generate gene expression profiles of fetal mammary cells with unique sorting strategies. These analyses reveal that sorting fetal mammary cells with Sox10 and EpCAM sorting markers provides a stroma-free fMaSC-enriched cell population. The gene expression profiling of these cells offers a resources to probe the molecular mechanisms that specify this unique cell state. Examination of 2 different sorting strategies for fetal mammary cells

2015-08-04 | E-GEOD-71635 | biostudies-arrayexpress

EZH2 controls mammary differentiation independently of its methyltransferase activity through controlling genomic STAT5 access

Project description:Mammary development is characterized by the proliferation and progressive differentiation of alveolar epithelium during pregnancy, culminating in lactation. These processes are largely controlled by hormones through transcription factors. We now explore the contributions of histone methyltransferases, which establish H3K27me3 marks, in the temporally-regulated differentiation of mammary epithelium. Loss of EZH2, but not EZH1, resulted in precocious mammary differentiation, which was facilitated by STAT5 binding to specific target genes and their activation. Mammary stem cells were not compromised in the absence of EZH2. Genome-wide H3K27me3 patterns remained intact in the absence of EZH2. Mammary-specific loci were devoid of H3K27me3 marks in mammary progenitor and mature cells, suggesting no regulatory role for this repressive mark. Lastly, the combined absence of EZH1 and EZH2 inhibited the formation of alveoli. Taken together, EZH2 controls temporally-restricted differentiation of mammary epithelium through H3K27me3-independent mechanisms. mRNA-seq and ChIP-seq in MMTV-Cre (Control), E1-/- (E1KO), E1+/-;E2f/f;control (E1+/-E2KO) and Ezh2f/f;control (E2KO) mammary gland tissues or MECs (purified mammary epithelial cells). H3K27me3 and STAT5 ChIP-seqs in mammary tissues at p13; H3K4me3 ChIP-seq in MECs (mammary epithelial cells) at p13; RNA-seqs at mature virgin (with/without prolactin injection), p13 and p18 mammary tissues.

2013-12-31 | E-GEOD-52016 | biostudies-arrayexpress

Sox10 regulates stem/progenitor and mesenchymal cell states in mammary epithelial cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-08-04 | E-GEOD-71300 | biostudies-arrayexpress

Inhibiting coronavirus replication by chemical ER stress, including SARS-CoV-2 and MERS-CoV

Project description:Coronaviruses (CoVs) are important human pathogens for which no specific treatment is available. Here, we provide evidence that pharmacological reprogramming of ER stress pathways can be exploited to suppress CoV replication. We found that the ER stress inducer thapsigargin efficiently inhibits coronavirus (HCoV-229E, MERS-CoV, SARS-CoV-2) replication in different cell types, (partially) restores the virus-induced translational shut-down, and counteracts the CoV-mediated downregulation of IRE1α and the ER chaperone BiP. Proteome-wide data sets revealed specific pathways, protein networks and components that likely mediate the thapsigargin-induced antiviral state, including HERPUD1, an essential factor of ER quality control, and ER-associated protein degradation complexes. The data show that thapsigargin hits a central mechanism required for CoV replication, suggesting that thapsigargin (or derivatives thereof) may be developed into broad-spectrum anti-CoV drugs.

2021-06-24 | PXD021222 | Pride

Expression data from mouse luminal mammary epithelial cells

Project description:We used a mouse strain in which one Tbx3 gene was replaced with the yellow fluorescent protein variant Venus. Luminal cells had either very high Tbx3 promoter activity or not at all. We performed an expression analysis on luminal mammary epithelial cells sorted based on their Venus expression (reporting Tbx3 promoter activity) to investigate the difference between these two cell populations. Mammary epithelial cells from 3 Tbx3-Venus-KI adult virgin female mice (FVB background) were pooled and luminal cells were sorted into a Venus-hi and a Venus-neg sample. There were no repeats for this study.

2014-08-20 | E-GEOD-58327 | biostudies-arrayexpress

Distinct STAT5 concentrations uniquely control establishment and differentiation of mammary epithelium during pregnancy

Project description:To dissect regulatory processes of cell proliferation and differentiation we generated mouse strains carrying any combination of the four Stat5 alleles, thus expressing STAT5 from 0 to 100%. RNA-Seq analyses revealed that different STAT5 levels activate specific genetic programs linked to cell proliferation and differentiation. We refer to wild-type mice and Stat5abfl/fl mice as AABB mice; Stat5abfl/fl;MMTV-Cre (with Stat5ab-deficient mammary epithelial cells) as Null mice; Stat5a-/- mice as BB mice; Stat5b-/- mice as AA mice; Stat5ab+/null mice as AB mice.

2012-05-02 | E-GEOD-37646 | biostudies-arrayexpress

An in vivo neuroimmune organoid model to study human brain environment-dependent microglia phenotypes

Project description:Characterization of human stem cell-derived microglia (hMG) that develop within vascularized human brain organoids under physiological conditions in vivo. We isolated tdT+/CD45+ hMG from five animals and three time points (6, 12 and 24 weeks post transplantation) using Fluorescence-activated cell sorting (FACS), following a strictly controlled ex vivo isolation procedure as previously described (Gosselin et al., 2017) and profiled those cells using single cell RNA sequencing.

2023-05-11 | E-MTAB-11522 | biostudies-arrayexpress

MiR-21 is targeted by STAT5 but dispensable for mammary gland development

Project description:In this study we identifies miR-21 to by under cytokine control through the transcription factor STAT5 and while miR-21 is differentially expressed during mammary gland development, miR-21 is dispensable for mammary development and lactation. We refer to wild-type mice (+/+) as WT and to mice lacking the mir-21 (-/-) as KO mice.

2013-08-22 | E-GEOD-50068 | biostudies-arrayexpress

Expression data from immature dendritic cells (iDC) expressing HIV-1 Tat alleles and mutants

Project description:HIV-1 Tat induces the expression of interferon (IFN)-inducible genes in immature dendritic cells (iDC) in the absence of IFN production. We evaluated how three alleles of Tat and some Tat mutants differ in cellular gene modulation and whether a similar gene induction pattern could be detected by treating cells with IFNM-bM-^@M-^Ys. The three alleles and mutants, with the exception of mutants TatSF21-47 and TatSF2G48-R57A that do not localize in the nucleous, modulated to different degrees IFN-inducible genes without concomitant induction of IFNM-bM-^@M-^Ys. The first exon TatSF21-72 and the minimal transactivator TatSF21-58, all induced genes to a significantly greater extent than full-length Tat. The 2nd exon appears to diminish the gene modulation that can be observed when the first exon alone is expressed. We investigated the effect of various Tat alleles and mutants on host cell gene expression in immature dendritic cells (iDC). The cells were infected with adenoviruses expressing the Tat constructs. The Tat alleles and mutants are under a tetracycline inducible promoter and are expressed only in cells co-infected with Ad-tTA, which expresses the tetracycline responsive transactivator. 10e6 iDC were infected with 5 plague forming units per cell of the adenoviruses and cells were collected 10 and 20 hours post-infection. RNA was isolated and mRNA expression levels were analyzed by microarrays. As controls we used cells that were left uninfected and cells that were infected with Ad-LacZ, which expresses beta-galactosidase.

2013-06-01 | E-GEOD-42924 | biostudies-arrayexpress

FASN-dependent de novo lipogenesis is required for brain development

Project description:Fate and behaviour of neural progenitor cells is tightly regulated during mammalian brain development. Metabolic pathways, such as glycolysis and oxidative phosphorylation, that are required for supplying energy and providing molecular building blocks to generate cells, govern progenitor function. However, the role of de novo lipogenesis, which is the conversion of glucose into fatty acids through the multi-enzyme protein fatty acid synthase (FASN), for brain development remains unknown. Using Emx1Cre-mediated, tissue-specific deletion of Fasn in the mouse embryonic telencephalon, we show that loss of FASN causes severe microcephaly, largely due to altered polarity of apical, radial glia progenitors (APs) and reduced progenitor proliferation. Further, genetic deletion and pharmacological inhibition of FASN in human embryonic stem cell (ESC)-derived forebrain organoids identifies a conserved role of FASN-dependent lipogenesis for radial glia cell polarity and progenitor expansion in the developing human forebrain. Thus, our data establish a role of de novo lipogenesis for mouse and human brain development and identify a link between progenitor cell polarity and lipid metabolism.

2022-01-14 | PXD026110 | Pride

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