Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transdifferentiation of B lymphocyte line ER1 into ter cells in vitro

ABSTRACT: Transdifferentiation of B lymphocyte line ER1 into ter cells in vitro

PROVIDER: PRJNA833465 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Transdifferentiation of B lymphocyte line ER1 into ter cells in vitro

Project description:CD19 + ER1 (B lymphocyte line) cells differentiated into CD45 + Ter119 + ter cells in vitro, we selected CD19 + ER1 cells (CD19+CD45+TER119-CD11b+), intermediate ER1 cells (CD19-CD45+TER119-CD11b+) and Ter119 + CD45 + CD19 - ER1 cells (CD19-CD45+TER119+CD11b+) for transcriptome analysis. We then performed gene expression profiling analysis using data obtained from RNA-seq of those 3 cell lines.

2022-05-02 | GSE201915 | GEO

A Runx1-enhancer element eR1 identified lineage restricted mammary luminal stem cells

Project description:Mammary gland homeostasis is maintained by adult tissue stem-progenitor cells residing within the luminal and basal epithelia. Dysregulation of mammary stem cells is a key mechanism for cancer development. However, stem cell characterization is challenging because reporter models using cell-specific promoters do not fully recapitulate the mammary stem cell populations. We previously found that a 270-basepair Runx1 enhancer element, named eR1, marked stem cells in the blood and stomach. Here, we identified eR1 activity in a rare subpopulation of the ERα-negative luminal epithelium in mouse mammary glands. Lineage-tracing using an eR1-CreERT2 mouse model revealed that eR1+ luminal cells generated the entire luminal lineage and milk-secreting alveoli – eR1 therefore specifically marks lineage-restricted luminal stem cells. eR1-targeted-conditional knockout of Runx1 led to the expansion of luminal epithelial cells, accompanied by elevated ERα expression. Our findings demonstrate a definitive role for Runx1 in the regulation of the eR1-positive luminal stem cell proliferation during mammary homeostasis. Our findings identify a mechanistic link for Runx1 in stem cell proliferation and its dysregulation in breast cancer. Runx1 inactivation is therefore likely to be an early hit in the cell-of-origin of ERα+ luminal type breast cancer.

2021-09-22 | GSE184481 | GEO

Identification of genes downregulated due to loss at 8p11.22-ter

Project description:In this study, we compared expression profiles between pancreatic cell lines with and without loss at 8p11.22-ter to identify genes downregulated due to loss at 8p11.22-ter.

2016-01-22 | GSE65176 | GEO

Exserohilum rostratum strain:ER1

Project description:Exserohilum rostratum strain:ER1 Genome sequencing and assembly

| PRJNA735857 | ENA

Embelia ribes isolate:ER1

Project description:Embelia ribes isolate:ER1 Genome sequencing and assembly

| PRJNA343859 | ENA

Curtobacterium sp. ER1/6

Project description:Curtobacterium sp. ER1/6 Genome sequencing and assembly

| PRJNA339451 | ENA

Methylobacterium oryzihabitans strain:TER-1

Project description:Methylobacterium oryzihabitans strain:TER-1 Genome sequencing and assembly

| PRJNA512505 | ENA

BRCA1 suppresses microhomology-mediated tandem duplications at Tus/Ter-stalled replication forks

Project description:Small ~10 kb microhomology-mediated tandem duplications (“Group 1 TDs”) are abundant in BRCA1-linked but not BRCA2-linked breast cancer genomes. Here, we define the mechanism underlying this rearrangement signature. We show that BRCA1, but not BRCA2, suppresses TDs at a Tus/Ter site-specific chromosomal replication fork barrier in primary mammalian cells. BRCA1 has no equivalent role at chromosomal double strand breaks, indicating specificity for the stalled fork response. Two motor proteins—FANCM and the Bloom’s syndrome helicase—suppress Tus/Ter-induced TDs in BRCA1 mutants, revealing the existence of a multi-gene TD suppressor network. TDs arise by a “replication restart-bypass” mechanism terminated by end joining or microhomology-mediated template switching, the latter forming complex TD breakpoints. We show that solitary DNA ends form directly at Tus/Ter, implicating misrepair of these lesions in TD formation. We find that BRCA1 inactivation is strongly associated with Group 1 TDs in ovarian cancer. The Group 1 TD phenotype may be a general signature of BRCA1-deficient cancer

2017-11-23 | GSE103624 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Ter cells Transcriptomes

Project description:Purpose:The purpose of this study is to detect genes Ter-119+CD45−Lin− cells sorted from spleen of tumor-bearing mice and the control cells. Gene expression differences between seven samples could be found using transcriptome profiling (RNA-seq) analysis. Methods: The seven cell subsets were isolated from spleen of tumor-bearing mice, embryonic liver (E14.5) and bone marrow of wild type mice by cell sorter respectively. Cells with purity >98% were used for subsequent experiments. The cell subsets RNA profiles were generated by deep sequencing,using Illumina. Results: Genes with FPKM values above 10.0 in the cell groups were used for subsequent analysis. Single linkage clustering analysis between the groups and prcomp function-based PCA analysis on the expression matrix were performed by R software. We found that the tumor-induced Ter-119+CD45−Lin− cells expressed the transcriptional factors and functional genes associated with erythrocyte and megakaryocyte development, but not myeloid cells differentiation.

2018-06-01 | GSE109429 | GEO

Analysis of transcriptional differences between TER cells, B lymphocytes and embryonic liver nucleated erythrocytes

Project description:To verify the origin of TER cells from B lymphocytes，we profiled the differentially expressed genes in CD19+/TER119+/CD45+ cells by RNA-sequencing, with fetal liver-derived CD71+/TER119+/FSChigh cells (CECs) as erythroblast control and CD19+/TER119- cells as B-cell control.

2022-05-03 | GSE201937 | 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