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accession-icon GSE74410
Prdm1
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal-foetal interface during pregnancy.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP065344
Single-cell RNA-seq transcriptome profiling of Prdm1+ lineages in E9.5 mouse placenta
  • organism-icon Mus musculus
  • sample-icon 77 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Our goal was to transcriptionally profile Prdm1+ cell lineages of maternal and embryonic origin in mid-gestation mouse placenta in order to study vascular mimicry and additional processes in the placenta. Overall design: Profiling of 61 single cells and 17 clusters of 2 or 3 cells chosen based on expression of Prdm1, a paternally inherited Prdm1-Venus fluorescent reporter, progenitor trophoblast marker Gjb3 and spiral artery trophoblast giant cell marker Prl7b1.

Publication Title

Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal-foetal interface during pregnancy.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE74409
Molecular function of Prdm1/Blimp1 in trophoblast giant cell differentiation.
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Expression profiling of wild-type and Prdm1 null mouse trophoblast giant cell cultures using Illumina whole genome mouse V2 arrays.

Publication Title

Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal-foetal interface during pregnancy.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP161807
Single cell RNA sequencing identifies unique inflammatory airspace macrophage subsets
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

In this study, we characterize transciprtional phenotypes of airway macrophagages (AMs) throughout homeostatsis, inflammation, and repair at single cell granularity. We confirm that cell origin is the major determinant of AM programing and describe two previously uncharacterized, transcriptionally distinct subdivisions of AMs based on proliferative capacity and inflammatory programing. Overall design: We stimulated mice with LPS and then sampled FACs sorted airway macrophage cells using BAL at Days 0, 3, and 6 and sequenced 1,134 cells from these three groups using RNA-seq

Publication Title

Single cell RNA sequencing identifies unique inflammatory airspace macrophage subsets.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE110164
Combinatorial Smad2/3 Activities Downstream of Nodal Signaling Maintain Embryonic/Extra-Embryonic Cell Identities during Lineage Priming
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Combinatorial Smad2/3 Activities Downstream of Nodal Signaling Maintain Embryonic/Extra-Embryonic Cell Identities during Lineage Priming.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE110058
Combinatorial Smad2/3 Activities Downstream of Nodal Signaling Maintain Embryonic/Extra-Embryonic Cell Identities during Lineage Priming [array]
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Epiblast cells in the early post-implantation stage mammalian embryo undergo a transition described as lineage priming before cell fate allocation, but signaling pathways acting upstream remain ill defined. Genetic studies demonstrate that Smad2/3 double-mutant mouse embryos die shortly after implantation. To learn more about the molecular disturbances underlying this abrupt failure, here we characterised Smad2/3-deificient embryonic stem cells (ESCs). We found that Smad2/3 double-knockout ESCs induced to form epiblast-like cells (EpiLCs) display changes in nave and primed pluripotency marker gene expression, associated with the disruption of Oct4-bound distal regulatory element. In the absence of Smad2/3, we observed enhanced Bmp target gene expression and de-repression of extra-embryonic gene expression. Cell fate allocation into all three embryonic germ lakers is disrupted. Collectively, these experiments demonstrate that combinatorial Smad2/3 functional activities are required to maintain distinct embryonic and/or extra-embryonic cell identity during lineage priming in the epiblast before gastrulation.

Publication Title

Combinatorial Smad2/3 Activities Downstream of Nodal Signaling Maintain Embryonic/Extra-Embryonic Cell Identities during Lineage Priming.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE70958
Molecular function of Lhx1 in early mouse development
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Lhx1 functions together with Otx2, Foxa2, and Ldb1 to govern anterior mesendoderm, node, and midline development.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE70956
Molecular function of Lhx1 in early mouse development (BeadChip)
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Expression profiling of wild-type and Lhx1 null mouse definitive endoderm cultures using Illumina whole genome mouse V2 arrays.

Publication Title

Lhx1 functions together with Otx2, Foxa2, and Ldb1 to govern anterior mesendoderm, node, and midline development.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP099085
Comparing murine lung resident alveolar Siglec-F(high) macrophages to CD11b(high) macrophages following bleomycin injury
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Macrophages (MF) have been shown to contribute to fibrogenesis, however the underlying mechanisms and specific MF subsets involved remain unclear. Lung MF can be divided into two subsets: Siglec-Fhi resident alveolar MF and CD11bhi MF that primarily arise from immigrating monocytes. RNA-seq analysis was performed to compare these MF subsets during fibrosis. CD11bhi MF, not Siglec-Fhi MF, expressed high levels of pro-fibrotic chemokines and growth factors. Overall design: C56BL/6 WT mice were treated intratracheally with bleomycin. 8 days later, CD64+Mertk+ MF were sorted into Siglec-F(high) and CD11b(high) subsets. SiglecF(high) MF from naïve mice were also sorted. RNA was isolated and RNA-seq was performed to compare MF subsets.

Publication Title

Deletion of c-FLIP from CD11b<sup>hi</sup> Macrophages Prevents Development of Bleomycin-induced Lung Fibrosis.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Treatment, Subject

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accession-icon SRP018859
Genome wide RNA-seq analysis of E9.5 Smchd1 wild type and mutant embryos
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the deregulation of expression in E9.5 male mouse embryos are that homozygous for a mutant allele of the Smchd1 gene (ie Smchd1MommeD1/MommeD1). Overall design: RNA-seq analysis of Smchd1+/+ vs Smchd1MommeD1/MommeD1

Publication Title

Smchd1 regulates a subset of autosomal genes subject to monoallelic expression in addition to being critical for X inactivation.

Sample Metadata Fields

Sex, Subject

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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