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E-MEXP-1597
Mus musculus
6 Downloadable Samples
Affymetrix Mouse Expression 430A Array (moe430a)
Description
Expression profile of FLA2 (highest LSC frequency) and FLB1 (lowest LSC frequency) leukemias.
Publication Title
A role for GPx3 in activity of normal and leukemia stem cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 134 Downloadable Samples
Illumina HiSeq 2000
Description
We analysed the transcriptome of different HSC-enriched subpopulations of cells sorted from human umbilical cord blood and isolated from several individuals with different genetic backgrounds. We aim at identifying new cell surface markers associated with human HSC and downstream mature hematopoietic cell activity. Overall design: RNA-seq of CD34+CD45RA- cord blood cells from 17 non-pooled individuals.
Publication Title
GPR56 identifies primary human acute myeloid leukemia cells with high repopulating potential in vivo.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 121 Downloadable Samples
- Illumina HiSeq 2000
Description
The goal of the study was to identify genes that are directly or indirectly coregulated by the AhR pathway in primary human AML cells. Patient AML cells were treated for 16 hours with the two indirubin derivatives 6-bromoindirubin-3''oxime (BIO), 1-Methyl-6-bromoindirubin-3''oxime (MeBIO), the AHR-antagonist SR1 (StemReginin1), combinations of BIO+SR1 and MeBIO+SR1 or DMSO alone at indicated concentrations prior to RNA extraction for sequencing. Overall design: RNA-Seq performed on 5 primary AML samples fresh (t0) and after exposure to AhR-agonists (2), -antagonist (1), and DMSO Contributor: Leucegene Project, IRIC
Publication Title
GPR56 identifies primary human acute myeloid leukemia cells with high repopulating potential in vivo.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 16 Downloadable Samples
- NextSeq 500
Description
Intracellular trafficking is essential for proper cell signaling. In the pancreas, secretory cells rely on trafficking to regulate blood glucose and digestion. Pancreatic disorders reflect defects in function or development, evoking considerable interest in understanding the molecular genetics governing pancreatic organogenesis. Here, we show the transcription factor NFIA regulates trafficking in both the embryonic and adult pancreas, affecting both developmental cell fate decisions and adult physiology. NFIA deletion from pancreatic progenitors led to the development of more acinar cells and ducts and fewer endocrine cells, whereas ectopic NFIA promoted endocrine formation. We found that NFIA's effects on trafficking influence endocrine/exocrine cell fate decisions through regulation of Notch. Adult NFIA-deficient mice develop diabetic phenotypes due to impaired insulin granule trafficking and defects in acinar zymogen secretion. This study shows how a single transcription factor, NFIA, thus exerts profound effects on both embryonic cell fate and adult physiology by regulating vesicle trafficking. Overall design: 2 control and 2 NFIA fl/fl; Pdx1-cre samples, from pooled embryonic litters at E17.5
Publication Title
Pancreatic Cell Fate Determination Relies on Notch Ligand Trafficking by NFIA.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Developmental regulation of gliogenesis in the mammalian CNS is incompletely understood, in part due to a limited repertoire of lineage-specific genes. We used Aldh1l1-GFP as a marker for gliogenic radial glia and later-stage precursors of developing astrocytes and performed gene expression profiling of these cells. We then used this dataset to identify candidate transcription factors that may serve as glial markers or regulators of glial fate. Our analysis generated a database of developmental stage-related markers of Aldh1l1+ cells between murine embryonic day 13.5-18.5. Using these data we identify the bZIP transcription factor Nfe2l1 and demonstrate that it promotes glial fate under direct Sox9 regulatory control. Thus, this dataset represents a resource for identifying novel regulators of glial development.
Publication Title
Expression profiling of Aldh1l1-precursors in the developing spinal cord reveals glial lineage-specific genes and direct Sox9-Nfe2l1 interactions.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We demonstrate for the first time that the extracellular matrix glycoprotein Tenascin-C regulates the expression of key patterning genes during late embryonic spinal cord development, leading to a timely maturation of gliogenic neural precursor cells. We first show that Tenascin-C is expressed by gliogenic neural precursor cells during late embryonic development. The loss of Tenascin-C leads to a sustained generation and delayed migration of Fibroblast growth factor receptor 3 expressing immature astrocytes in vivo. Furthermore, we could demonstrate an upregulation of Nk2 transcription factor related locus 2 (Nkx2.2) and its downstream target Sulfatase 1 in vivo. A dorsal expansion of Nkx2.2-positive cells within the ventral spinal cord indicates a potential progenitor cell domain shift. Moreover, Sulfatase 1 is known to regulate growth factor signalling by cleaving sulphate residues from heparan sulphate proteoglycans. Consistent with this possibility we observed changes in both Fibroblast growth factor 2 and Epidermal growth factor responsiveness of spinal cord neural precursor cells. Taken together our data clearly show that Tenascin-C promotes the astroglial lineage progression during spinal cord development.
Publication Title
The extracellular matrix molecule tenascin C modulates expression levels and territories of key patterning genes during spinal cord astrocyte specification.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The intestinal immune system must elicit robust immunity against harmful pathogens but restrain immune responses directed against commensal microbes and dietary antigens. The mechanisms that maintain this dichotomy are poorly understood. Here we describe a population of CD11b+F4/80+CD11c macrophages in the lamina propria (LP) that express several anti-inflammatory molecules including interleukin 10 (IL-10), but little or no pro-inflammatory cytokines, even upon stimulation with Toll-like receptor (TLR) ligands. These macrophages induced, in a manner dependent on IL-10, retinoic acid and exogenous transforming growth factor-, differentiation of FoxP3+ regulatory T cells. In contrast, LP CD11b+ dendritic cells elicited IL-17 production. This IL-17 production was suppressed by LP macrophages, indicating that a dynamic interplay between these subsets may influence the balance between immune activation and tolerance.
Publication Title
Lamina propria macrophages and dendritic cells differentially induce regulatory and interleukin 17-producing T cell responses.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 30 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Activation of inflammatory pathways in human IBD
Publication Title
Activation of an IL-6:STAT3-dependent transcriptome in pediatric-onset inflammatory bowel disease.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 39 Downloadable Samples
- Illumina Genome Analyzer
Description
As a starting point for dissecting the cellular heterogeneity of gliomas, different subpopulations from a CRISPR mouse model of glioma were profiled for gene expression. Because we initially identified these astrocyte subpopulations in the mouse brain, we first sought to determine whether their malignant analogues are present in mouse models of glioma. Towards this, we recently developed a mouse model of malignant glioma, one that utilizes E16.5 IUE approaches in combination with CRISPR mediated gene editing, where we use IUE to introduce gRNA vectors to delete NFI, PTEN, and p53, CAS9, and a GFP reporter, resulting in the generation of malignant glioma at P70. Using the GFP label to distinguish tumor from normal brain tissue, along with FACS-based selection against the glioma stem cell (GSC) and endothelial cells (see methods), we screened our tumor models for the presence of these prospective astroglial populations in the non-GSC fractions of these tumors. Overall design: Gene expression profiles (by RNA-seq) were taken of mouse glioma cells of three different populations.
Publication Title
Identification of diverse astrocyte populations and their malignant analogs.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Pathological bone changes differ considerably between inflammatory arthritic diseases, and most studies have focused on bone erosion. Collagen Induced Arthritis (CIA) is a model for Rheumatoid Arthritis, which, in addition to bone erosion, demonstrates bone formation at the time for clinical manifestations. The objective of this study was to use the CIA model to study bone remodelling by performing a gene expression profiling time-course study on the CIA model.
Publication Title
Kinetics of gene expression and bone remodelling in the clinical phase of collagen-induced arthritis.
Sample Metadata Fields
Specimen part
View Samples