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accession-icon GSE65721
RelA Nuclear factor-kappaB (NF-kB) Subunit binding Loci in Promoter Regions of PHM1-31 Myometrial Smooth Muscle Cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Binding loci of RelA-containing nuclear factor-kappaB dimers in promoter regions of PHM1-31 myometrial smooth muscle cells.

Alternate Accession IDs

E-GEOD-65721

Sample Metadata Fields

Specimen part

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accession-icon E-MEXP-209
Transcription profiling of wounds from ovariectomized MIF null mice and controls to investigate the role of MIF during wound healing using BALB/C MIF null mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The 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.

Publication Title

Macrophage migration inhibitory factor: a central regulator of wound healing.

Alternate Accession IDs

None

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE65707
RelA Nuclear factor-kappaB (NF-kB) Subunit binding Loci in Promoter Regions of PHM1-31 Myometrial Smooth Muscle Cells (expression)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A 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.

Publication Title

Binding loci of RelA-containing nuclear factor-kappaB dimers in promoter regions of PHM1-31 myometrial smooth muscle cells.

Alternate Accession IDs

E-GEOD-65707

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP049302
Thymic T-cell progenitor development is supported by membrane bound Kit ligand provided by a combined vascular endothelial and epithelial niche.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Gene 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

Publication Title

A dynamic niche provides Kit ligand in a stage-specific manner to the earliest thymocyte progenitors.

Alternate Accession IDs

GSE62741

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE95012
Loss of Cic leads to aberrant neural stem cell proliferation and differentiation and promotes gliomagenesis
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Mouse 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.

Publication Title

<i>Cic</i> Loss Promotes Gliomagenesis via Aberrant Neural Stem Cell Proliferation and Differentiation.

Alternate Accession IDs

E-GEOD-95012

Sample Metadata Fields

Specimen part

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accession-icon GSE54219
Molecular genomic and transcriptomic profiling of familial breast cancer.
  • organism-icon Homo sapiens
  • sample-icon 155 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genomic profiling of CHEK2*1100delC-mutated breast carcinomas.

Alternate Accession IDs

E-GEOD-54219

Sample Metadata Fields

Specimen part

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accession-icon GSE88828
Effects of IDH1-R132H on mouse neural stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Mouse 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

Publication Title

Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression.

Alternate Accession IDs

E-GEOD-88828

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP067537
Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

One 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.

Publication Title

Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses.

Alternate Accession IDs

GSE76132

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP156577
RNA sequencing of genetically engineered mouse model lung tumors and normal mouse lung.
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Genetically 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.

Publication Title

The Lineage-Defining Transcription Factors SOX2 and NKX2-1 Determine Lung Cancer Cell Fate and Shape the Tumor Immune Microenvironment.

Alternate Accession IDs

GSE118246

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP156576
Single-cell RNA-sequencing of tumor associated neutrophils and control peripheral blood neutrophils in a novel lung squamous cell carcinoma mouse model
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Tumor-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.

Publication Title

The Lineage-Defining Transcription Factors SOX2 and NKX2-1 Determine Lung Cancer Cell Fate and Shape the Tumor Immune Microenvironment.

Alternate Accession IDs

GSE118245

Sample Metadata Fields

Specimen part, 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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