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Mus musculus
48 Downloadable Samples
Description
The regulatory logic underlying global transcriptional programs controlling development of visceral organs like the pancreas remains undiscovered. Here, we profiled gene expression in 12 purified populations of fetal and adult pancreatic epithelial cells representing crucial progenitor cell subsets, and their endocrine or exocrine progeny. Using probabilistic models to decode the general programs organizing gene expression, we identified co-expressed gene modules in cell subsets that revealed patterns and processes governing progenitor cell development, lineage specification, and endocrine cell maturation. Module network analysis linked established regulators like Neurog3 to unrecognized roles in endocrine secretion and protein transport, and nominated multiple candidate regulators of pancreas development. Phenotyping mutant mice revealed that candidate regulatory genes encoding transcription factors, including Bcl11a, Etv1, Prdm16 and Runx1t1, are essential for pancreas development or glucose control. Our integrated approach provides a unique framework for identifying regulatory networks underlying pancreas development and diseases like diabetes mellitus.
Publication Title
An integrated cell purification and genomics strategy reveals multiple regulators of pancreas development.
Alternate Accession IDs
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
Description
Genome-wide comparative gene expression analysis of callus tissue of osteoporotic mice (Col1a1-Krm2 and Lrp5-/-) and wild-type were performed to identify candidate genes that might be responsible for the impaired fracture healing observed in Col1a1-Krm2 and Lrp5-/- mice.
Publication Title
Osteoblast-specific Krm2 overexpression and Lrp5 deficiency have different effects on fracture healing in mice.
Alternate Accession IDs
Sample Metadata Fields
Sex, Age, Specimen part
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GSE10849- Mus musculus
- 6 Downloadable Samples
Description
Hearts Lacking Caveolin-1 Develop Hypertrophy with Normal Cardiac Substrate Metabolism
Publication Title
Hearts lacking caveolin-1 develop hypertrophy with normal cardiac substrate metabolism.
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
Description
The aim of this study was to determine the effect of transgenic Aire expression on the transcriptional profile of a tissue that normally does not express Aire: pancreatic islets. The transcriptional profile of transgenic RIP-Aire27 islets was compared to non-transgenic littermate islets as well as to archival NOD thymic medullary epithelial cells (MEC) data. All data were from non-obese diabetic (NOD) mice
Publication Title
Transcriptional impact of Aire varies with cell type.
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
Description
RAS oncogenic mutations are common in human cancers, but RAS proteins have been difficult to target. We sought to identify pharmacological agents to block the RAS oncogenic signaling by a distinct mechanism. Since the biological activity of RAS proteins rely upon lipid modifications and RAS regulates lipid metabolisms in cancer cells, we screened a bioactive lipid library using a RAS specific cell viability assay. We report the discovery of a new class of inhibitors for RAS transformation. Compounds in the class represented by endocannabinoid N-arachidonoyl dopamine (NADA) can induce cell oncosis, independent of its ability to engage cannabinoid receptors. Further analyses show that NADA is more active in inhibiting the NRAS transformation and signaling than that of KRAS4B. Mechanistically, NADA blocks the plasma membrane translocation of NRAS, but not that of KRAS4B. In addition, NADA inhibits the plasma membrane translocation and neoplastic transformation of oncogenic KRAS4A. Interestingly, NADA also redistributes the cytoplasmic NRAS to the Golgi apparatus in a palmitoylation-dependent manner. The results indicate that NADA inhibits NRAS and KRAS4A plasma membrane translocation by targeting a novel molecular process. The new findings would help to develop novel targeted therapies for a broad range of human cancers.
Publication Title
N-Arachidonoyl Dopamine Inhibits NRAS Neoplastic Transformation by Suppressing Its Plasma Membrane Translocation.
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 7 Downloadable Samples
Description
Following the identification of a critical time window of Blood Brain Barrier formation in the mouse embryo, we aimed to identify genes important for barriergenesis. To this end, we isolated cortical and lung E13.5 endothelial cells and compared expression between the two populations.
Publication Title
Mfsd2a is critical for the formation and function of the blood-brain barrier.
Alternate Accession IDs
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Reprogramming of the microRNA transcriptome mediates resistance to rapamycin.
Alternate Accession IDs
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
Description
The mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation. Inhibitors of mTOR are being evaluated as anti-tumor agents. Given the emerging role of microRNAs (miRNAs) in tumorgenesis we hypothesized that miRNAs could play important roles in the response of tumors to mTOR inhibitors. Rapamycin resistant myogenic cells developed by long-term rapamycin treatment showed extensive reprogramming of miRNAs expression, characterized by up-regulation of the mir-17~92 and related clusters and down-regulation of tumor-suppressor miRNAs. Antagonists of oncogenic miRNA families and mimics of tumor suppressor miRNAs (let-7) restored rapamycin sensitivity in resistant tumor cells. This study identified miRNAs as new downstream components of the mTOR-signaling pathway, which may determine the response of tumors to mTOR inhibitors.
Publication Title
Reprogramming of the microRNA transcriptome mediates resistance to rapamycin.
Alternate Accession IDs
Sample Metadata Fields
Specimen part, Cell line
View Samples- Danio rerio
- 2 Downloadable Samples
IlluminaGenomeAnalyzerII
Description
Precise 5' splice site recognition is essential for both constitutive and regulated pre-mRNA splicing. The U1 snRNP specific protein U1C is involved in this first step of spliceosome assembly and important for stabilizing early splicing complexes. We used an embryonically lethal U1C knockout mutant zebrafish, hi1371, to investigate the potential genomewide role of U1C for splicing regulation. Surprisingly, genomewide RNA-Seq analysis of mutant versus wildtype embryos revealed a large set of specific target genes that changed their alternative splicing patterns in the absence of U1C. In sum, our findings provide evidence for a new role of a general snRNP protein, U1C, as a mediator of alternative splicing regulation.
Publication Title
RNA-Seq analysis in mutant zebrafish reveals role of U1C protein in alternative splicing regulation.
Alternate Accession IDs
None
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 57 Downloadable Samples
Description
In order to understand how biochemical and genetic differences correlate with treatment response, we measured depressive-like behavior, gene expression and the levels of thirty-six neurobiochemical analytes across a panel of genetically-diverse mouse inbred lines after chronic treatment with vehicle or fluoxetine. Neurobiochemical markers were chosen based on their putative molecular function within pathways proposed to underlie depression, which include neuronal transmission, HPA-axis regulation, and neuroimmune processes. The goal of this study is to establish genetic and biochemical biomarkers that can predict treatment response and to propose a molecular pathway that is critical in mediating anti-depressant response.
Publication Title
Evaluating genetic markers and neurobiochemical analytes for fluoxetine response using a panel of mouse inbred strains.
Alternate Accession IDs
Sample Metadata Fields
Sex, Specimen part
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