This SuperSeries is composed of the SubSeries listed below.
Binding loci of RelA-containing nuclear factor-kappaB dimers in promoter regions of PHM1-31 myometrial smooth muscle cells.
Specimen part
View SamplesThe aim of this experiment was to investigate the role of MIF during wound healing using BALB/C MIF null mice and in the context of reduced estrogen-associated impaired healing using ovariectomized mice (a mouse model of age-associated delayed healing). Ageing is associated with delayed cutaneous wound healing resulting from reduced estrogen levels. Macrophage migration inhibitory factor (MIF - NCBI RefSeq: NM_010798) is thought to mediate the effects of estrogen on wound healing. Gene expression was compared between wounds from ovariectomized MIF null mice and controls.
Macrophage migration inhibitory factor: a central regulator of wound healing.
Sex, Age, Specimen part, Subject
View SamplesA study to define the binding loci of RelA-containing NF-kappaB dimers and subsequent correlation with gene expression in a human myometrial smooth muscle cell line after exposure to TNF.
Binding loci of RelA-containing nuclear factor-kappaB dimers in promoter regions of PHM1-31 myometrial smooth muscle cells.
Specimen part
View SamplesGene expression analysis of purified KitL-tomato+ and KitL-tomato- thymic vascular endothelial cells, cortical and medullary thymic epithelial cells from 5 weeks old male kitL-tomato reporter mice Overall design: Differentially expressed genes analysis of thymic stromal cells
A dynamic niche provides Kit ligand in a stage-specific manner to the earliest thymocyte progenitors.
No sample metadata fields
View SamplesMouse neural stem cells were generated from conditional knockout mice (Cicflox/flox) or the wild trype control mice (Cic+/+). Cic is conditionally knocked out following expression of Cre-recombinase. Cre-recombinase was incorporated in vitro via adenoviral-Cre transduction.
<i>Cic</i> Loss Promotes Gliomagenesis via Aberrant Neural Stem Cell Proliferation and Differentiation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genomic profiling of CHEK2*1100delC-mutated breast carcinomas.
Specimen part
View SamplesMouse neural stem cells were generated from conditional knock-in mice. Mutant IDH1 is conditionally expressed following expression of Cre-recombinase. Cre-recombinase was incorporated in vitro
Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression.
Specimen part
View SamplesOne of the most common genetic alterations in acute myeloid leukemia is the internal tandem duplication (ITD) in the FLT3 receptor for cytokine FLT3 ligand (FLT3L). The constitutively active FLT3-ITD promotes the expansion of transformed progenitors, but also has pleiotropic effects on normal hematopoiesis. We analyzed the effect of FLT3-ITD on dendritic cells (DCs), which express FLT3 and can be expanded by FLT3L administration. We report that young pre-leukemic mice with the Flt3ITD knock-in allele manifest an expansion of all DCs including classical (cDCs) and plasmacytoid (pDCs). The expansion originated in DC progenitors, occurred in a cell-intrinsic manner and was further enhanced in Flt3ITD/ITD mice. The mutation caused the downregulation of Flt3 on the surface of DCs and reduced their responsiveness to Flt3L. Flt3ITD mice showed enhanced capacity to support T cell proliferation, including a cell-extrinsic expansion of regulatory T cells (Tregs). Accordingly, these mice restricted alloreactive T cell responses during graft-versus-host reaction, but failed to control autoimmunity in the absence of Tregs. Thus, the FLT3-ITD mutation directly affects DC development, thereby indirectly modulating T cell homeostasis and supporting Treg expansion. This effect of FLT3-ITD may subvert immunosurveillance and promote leukemogenesis in a cell-extrinsic manner. Overall design: Sorted splenic dendritic cell subsets from either Flt3+/+ or Flt3ITD/+ mice were sequenced for mRNA profiling. For each subset per genotype contains 2-3 replicates, all from independent experiments.
Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses.
Specimen part, Cell line, Subject
View SamplesGenetically engineered mouse models (GEMM) of cancer are powerful tools to study multiple aspects of caner biology. We developed a novel GEMM for lung squamous cell carcinoma (LSCC) by genetically combining overexpression of Sox2 with loss of Lkb1: Rosa26LSL-Sox2-IRES-GFP;Lkb1fl/fl (SL). We compared gene expression profiles of SL lung tumors with normal mouse lung tissue, mouse lung adenocarcinoma (LADC) tumors from KrasLSL-G12D/+;Trp53fl/fl (KP), mouse LSCC tumors from Lkb1fl/fl;Ptenfl/fl (LP) model as well as Lenti-Sox2-Cre Lkb1fl/fl. Overall design: Tumors were isolated from formalin-fixed paraffin-embedded (FFPE) tissue samples by microdissection and nucleic acid isolation was performed followed by single-read or paired-end RNA sequencing.
The Lineage-Defining Transcription Factors SOX2 and NKX2-1 Determine Lung Cancer Cell Fate and Shape the Tumor Immune Microenvironment.
Specimen part, Subject
View SamplesTumor-associated neutrophils (TANs) can be conditioned to become “N2” pro-tumorigenic neutrophils in the tumor microenvironment. TANs have been shown to acquire N2 features and promote multiple aspects of tumor growth in mouse models of many cancers, including non-small cell lung cancer. We developed a novel mouse model for lung squamous cell carcinoma (LSCC): Rosa26LSL-Sox2-IRES-GFP;Nkx2-1fl/fl;Lkb1fl/fl (SNL). SNL mice develop tumors with short latency of ~3 months and SNL tumors have high neutrophil infiltration similar to other LSCC mouse models. We employed this novel model and single-cell RNA-sequencing to profile TANs in SNL lung tumors in comparison to peripheral blood neutrophils (PBNs) from tumor-bearing SNL mice. Overall design: Flow cytometry sorted neutrophils (CD45+CD11B+LY6G+) from freshly isolated SNL lung tumors or peripheral blood from tumor-bearing mice were single-cell RNA sequenced with 10X Genomics.
The Lineage-Defining Transcription Factors SOX2 and NKX2-1 Determine Lung Cancer Cell Fate and Shape the Tumor Immune Microenvironment.
Specimen part, Subject
View Samples