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Expression data from adult lungs isolated from TMEM100-deficient mice

ABSTRACT: Tmem100 was identified as a downstream gene of BMP9-ALK1 signaling. The signaling has been implicated in hereditary hemorrhagic telangiectasia. This study was designed to identify affected genes in TMEM100-deficiect mice. Tmem100 was inactivated in adult Tmem1002loxP/2loxP;ROSA26+/CreER mice by tamoxifen tereatment. Microarray data was obtained from the lungs isolated from tamoxifen treated control and mutant mice. Three control mice (Tmem1002loxP/2loxP) and three mutant mice (Tmem1002loxP/2loxP;ROSA26+/CreER) were treated with tamoxifen (two consecutive intraperitoneal injections, 0.1 mg/g of body weight) to activate CreER recombinase. Total RNAs were isolated from lungs 7 days after tamoxifen injection.

ORGANISM(S): Mus musculus

SUBMITTER: Young Jae Lee

PROVIDER: E-GEOD-57256 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from adult lungs isolated from TMEM100-deficient mice

Project description:Tmem100 was identified as a downstream gene of BMP9-ALK1 signaling. The signaling has been implicated in hereditary hemorrhagic telangiectasia. This study was designed to identify affected genes in TMEM100-deficiect mice. Tmem100 was inactivated in adult Tmem1002loxP/2loxP;ROSA26+/CreER mice by tamoxifen tereatment. Microarray data was obtained from the lungs isolated from tamoxifen treated control and mutant mice.

2014-05-03 | GSE57256 | GEO

Impact of IRP deficiency on the proteome of Ly6G+ cells from the bone marrow in mice

Project description:The overall objective of the project is to evaluate the effects of loss of function of iron regulatory proteins (IRP1, encoded by Aco1)-1 and -2 (IRP2, encoded by Ireb2) during adult life. Mice carrying floxed Aco1 and Ireb2 alleles were crossed to a knockin strain expressing a tamoxifen-inducible CRE recombinase under the control of the Rosa26 promoter. The resulting Aco1flox/flox,Ireb2flox/flox,Rosa26+/CreERT2 mice are designated P1/2-KO; littermates lacking the CreER sequence (Aco1flox/flox,Ireb2flox/flox,Rosa26+/+) serve as reference and are designated P1/2-CTR. Adult mice were injected (i.p.) with tamoxifen on day 1 and day 3 to ablate the IRPs in the whole body, and were sacrificed on day 10 for analysis. Bone marrow cells were collected and LY6G+ cells were magnetically sorted for proteome analysis by LC-MS/MS using an Ultimate 3000 UPLC system connected to an Orbitrap Exploris 480 mass spectrometer.

2023-03-11 | PXD032077 | Pride

Identification of Sox9-Regulated Pathways During the Secondary Transition Stage of Pancreas Development

Project description:Sox9 target genes were identified during the secondary transition stage of pancreas development by comparing gene expression in Sox9-ablated versus wild-type pancreata using microarray analysis. Sox9 was conditionally ablated during the secondary transition in the developing pancreas via recombination of a Sox9-flox allele (Kist et al., 2002) using the tamoxifen-inducible Rosa26-CreER allele (Vooijs et al., 2001). Dams were injected with 6 mg/40 g tamoxifen in corn oil at e12.5. Pancreata were manually microdissected at e15.5. Total RNA was isolated and pooled from pancreata of e15.5 Sox9fl/fl; Rosa26-CreER (mutant) versus Rosa26-CreER (wild-type) littermates for four biological replicates.

2012-08-01 | E-GEOD-28670 | biostudies-arrayexpress

Single-Cell RNA-sequencing of lung mesenchymal cells at multiple time points after bleomycin injury

Project description:Mesenchymal cells (CD31-, CD45-, EpCAM-, Ter119-) were collected for 10x Genomics Chromium Single Cell v3.1 scRNA-seq from the lungs of Scube2-CreER/Rosa26-tdTomato double homozygous mice on day 0 , 7, 14, 21 after bleomycin treatment.

2024-04-18 | GSE210341 | GEO

Single-cell RNA sequencing of self-maintaining lamina propria macrophages

Project description:Single-cell RNA sequencing of 697 YFP+ CD64+ lamina propria macrophages isolated from Cx3cr1CreERT2.Rosa26-LSL-YFP mice 35 weeks after tamoxifen administration

2018-07-30 | E-MTAB-6976 | biostudies-arrayexpress

Gene expression profile of mature plasmacytoid dendritic cells (PDC) after the deletion of transcription factor E2-2

Project description:The interferon-producing plasmacytoid dendritic cells (PDC) share common progenitors with antigen-presenting classical dendritic cells (cDC), yet they possess distinct morphology and molecular features resembling those of lymphocytes. It is unclear whether the unique cell fate of PDC is actively maintained in the steady state. We report that the deletion of transcription factor E2-2 from mature peripheral PDC caused their spontaneous differentiation into cells with cDC properties. This included the loss of PDC markers, increase in MHC class II expression and T cell priming capacity, acquisition of dendritic morphology and induction of cDC signature genes. Genome-wide chromatin immunoprecipitation revealed direct binding of E2-2 to key PDC-specific and lymphoid genes, as well as to certain genes enriched in cDC. Thus, E2-2 actively maintains the cell fate of mature PDC and opposes the “default” cDC fate, in part through direct regulation of lineage-specific gene expression programs. Inducible deletion of E2-2 (Tcf4) has been performed by administering tamoxifen to conditional E2-2flox/flox Rosa26-CreER+ mice or to E2-2flox/flox Rosa26-CreER- control littermates. Four or six days later total splenocytes were isolated, pooled from 2-3 mice and PDC (CD11b- B220+ CD11clow Bst2+) were isolated by sorting. Global gene expression profiles of E2-2-deficient (null) and control (Ctrl) PDC were compared using Affymetrix microarrays (GPL1261).

2010-12-21 | E-GEOD-24726 | biostudies-arrayexpress

Musashi proteins are post-transcriptional regulators of the epithelial-luminal cell state

Project description:mRNA-seq and ribosome profiling of neural stem cells overexpressing or knocked out for Musashi RNA-binding proteins Study of the global effects of Musashi (Msi) proteins on the transcriptome of embryonic neural stem cells. Neural stem cells were derived from brains of E12.5 or E13.5 embryos engineered to have inducible Msi1 or Msi2 genes, or from embryos with double floxed alleles of Msi1 and Msi2 carrying a Tamoxifen-induclble Cre (CreER). The overexpression mice were made using the Flp-in system (OpenBioSystems), where a cDNA of interest (in this case Msi1 or Msi2) is knocked into the Collagen (Col1A1) locus. The expression of the cDNA of interest is driven by m2rTTA that is knocked into the Rosa26 locus (R26). KH2 describes a strain containing the R26-m2rTTA but lacking Msi1 or Msi2 cDNA. MSI1 describes a strain containing R26-m2rTTA and Msi1 cDNA in Col1A1. MSI2 describes a strain containing R26-m2rTTA and Msi2 cDNA in Col1A1. C1 describes a strain lacking the CreER allele but containing double floxed alleles of Msi1/Msi2 (used as Tamoxifen control). C4 describes a strain carrying the CreER allele and double floxed alleles of Msi1/Msi2.

2014-06-13 | E-GEOD-58423 | biostudies-arrayexpress

Activation of a neural stem cell transcriptional program in parenchymal astrocytes

Project description:Neural stem cells, located in discrete niches in the adult brain, generate new neurons throughout life. These stem cells are specialized astrocytes, but astrocytes in other brain regions (parenchymal astrocytes) do not generate neurons under physiological conditions. After stroke, however, astrocytes in the mouse striatum undergo neurogenesis, triggered by decreased Notch signaling. Notch signaling can be experimentally depleted in mice by deleting the Notch-mediating transcription factor Rbpj. This dataset consists of single-cell RNA sequencing data of astrocytes isolated from the striatum (where astrocytes undergo neurogenesis in response to Rbpj deletion) or somatosensory cortex (where astrocytes don't complete neurogenesis in response to Rbpj deletion) of 4 mice. Cells were isolated from Cx30-CreER; R26-tdTomato; Rbpj(fl/fl) mice at three time points after tamoxifen-induced Rbpj deletion (2, 4, 8 weeks), and from Cx30-CreER; R26-tdTomato mice with intact Rbpj 3 days after tamoxifen. These time points span the transition from astrocyte through transit-amplifying cells to neuroblasts. The dataset contains 1) astrocytes from the striatum that initiate a neurogenic transcriptional program in response to Rbpj deletion and generate transit-amplifying cells and neuroblasts, and 2) astrocytes from the somatosensory cortex that initiate a neurogenic program in response to Rbpj deletion but fail to generate transit-amplifying cells or neuroblasts.

2020-08-01 | E-MTAB-9268 | biostudies-arrayexpress

Gene expression changes in Apc-mutant mouse intestinal organoids with and without deleting the Prox1 transcription factor

Project description:We isolated and selected intestinal adenoma organoids from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox mice and added tamoxifen to induce the deletion of the Apc and Prox1 genes in the intestinal epitheliul ex vivo. Microarray experiments were carried out 7 days after the addition of tamoxifen. Total RNA obtained from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox organoids were compared 7 days after the addition of tamoxifen and 5 days after the selection for Apc-mutant organoids in the absence of the Wnt-agonist R-Spondin1.

2014-08-15 | E-GEOD-47568 | biostudies-arrayexpress

Gene expression profiling of Scgb1a1+, CD24low cells isolated from the lungs of Scgb1a1-CreER; Rosa26-mTmG mouse.

Project description:We established a new method to find out subpopulation of lung epithelial stem cells, named scMORN, and uncovered the existence of Club cell subpopulations contributing to alveolar regeneration. We isolated entire Club cells by sorting Scgb1a1+, CD24low cells from the lungs of Scgb1a1-CreER; Rosa26-mTmG mouse. The gene expression profiling revealed that two genetically distinct types of Club cells.

2023-08-23 | GSE189917 | GEO

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