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GSE31666
Mus musculus
2 Downloadable Samples
Description
DNA damage plays a major role in neural cell death by necrosis and/or apoptosis. However, our understanding of the molecular mechanisms of neural cell death remains still incomplete. To acquire a global understanding of the various mediators related to DNA damage-induced neural cell death pathways, we performed a whole genomic wide screen in neural stem cells by using a siRNA library. We identified 80 genes required for DNA damage-induced cell death. 14 genes (17.5%) are directly related to cell death and/or apoptosis. 66 genes have not been previously directly linked to DNA damage-induced cell death. Using an integrated approach with functional and bioinformatics analysis, we have uncovered a molecular network containing several partially overlapping and interconnected pathways and/or protein complexes that are required for DNA damage-induced neural cell death. The identification of the network of neural cell death mediators will greatly enhance our understanding of the molecular mechanisms of neural cell death and provide therapeutic targets for nervous system disorders.
Publication Title
High-Content Genome-Wide RNAi Screen Reveals <i>CCR3</i> as a Key Mediator of Neuronal Cell Death.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 9 Downloadable Samples
Description
The role of Tfr1 in non-erythroid tissues remains elusive due to the embryonic lethality of the Tfr1 global knockout mouse model. To bypass this problem, we generated a mouse model in which Tfr1 was conditionally deleted in intestinal epithelial cells (IECs). These mice developed severe IEC disruption, characterized by blunted villi, edema, loss of proliferative intervillus IECs, accumulation of lipids, and early neonatal lethality. Strikingly, a wide range of genes associated with epithelial-to-mesenchymal transition were highly upregulated in IEC lacking Tfr1. Additionally, candidate vesicular transport and sorting genes implicated in lipid absorption and trafficking were downregulated. Surprisingly, the presence of a mutant allele of Tfr1, which is unable to bind to iron-loaded transferrin, was capable of rescuing the lethality, intestinal epithelial homeostasis, and proliferation in a majority of the Tfr1 conditional knockout mice.
Publication Title
Noncanonical role of transferrin receptor 1 is essential for intestinal homeostasis.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Homo sapiens
- 72 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.
Sample Metadata Fields
Age, Specimen part, Disease
View Samples- Mus musculus
- 39 Downloadable Samples
Description
Liver global gene expression patterns of 9 GNMT-knockout mice histopathologically determined to have non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) together with 10 MAT1A-knockout mice histopathologically determined to have steatosis and NASH. All these have their respective wild type patterns. These were analyzed to define signatures to study the pathogenesis of NAFLD-derived HCC, explore which subtypes of cancers can be investigated using mouse models and define a signature of HCC differential survival that can be used to characterize HCC subtypes of different survival derived from mixed etiologies.
Publication Title
Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.
Sample Metadata Fields
Age, Specimen part, Disease
View Samples- Danio rerio
- 1 Downloadable Sample
Description
Zebrafish have the remarkable ability to regenerate body parts including the heart, spinal cord and fins by a process referred to as epimorphic regeneration. Recent studies have illustrated that similar to adult zebrafish, early life stage-larvae also possess the ability to regenerate the caudal fin. A comparative genomic analysis was used to determine the degree of conservation in gene expression among the regenerating adult caudal fin, adult heart and larval fin. Results indicate that these tissues respond to amputation/injury with strikingly similar genomic responses. Comparative analysis revealed raldh2, a rate-limiting enzyme for the synthesis of Retinoic acid (RA), as one of the highly induced genes across the three regeneration platforms.
Publication Title
Comparative expression profiling reveals an essential role for raldh2 in epimorphic regeneration.
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.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Our laboratory wanted to define the transcription profile of aged skeletal muscle. For this reason, we performed a triplicate microarray study on young (3 weeks) and aged (24 months) gatrocnemius muscle from wild-type C57B16 Mice
Publication Title
Transcriptional profiling of skeletal muscle reveals factors that are necessary to maintain satellite cell integrity during ageing.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 111 Downloadable Samples
Description
Skeletal muscle atrophy is a consequence of many diseases, environmental insults, inactivity, age and injury. Atrophy is characterized by active degradation and removal of contractile proteins and a reduction in fiber size. Animal models have been extensively used to identify pathways leading to atrophic conditions. Here we have used genome-wide expression profiling analysis and quantitative PCR to identify the molecular changes that occur in two clinically relevant animal mouse models of muscle atrophy, hindlimb casting and Achilles tendon laceration (tenotomy). Gastrocnemius muscle samples were collected 2, 7 and 14 days after insult. The total amount of muscle loss as measured by wet weight and muscle fiber size was equivalent between models, although tenotomy resulted in a more rapid induction of muscle atrophy. Furthermore, tentomy resulted in the regulation of significantly more mRNA transcripts then casting. Analysis of the regulated genes and pathways suggest that the mechanism of atrophy is distinct between these models. The degradation following casting appears ubiquitin-proteasome-mediated while degradation following tenotomy appears lysosomal and matrix-metalloproteinase (MMP)-mediated. This data suggests that there are multiple mechanisms leading to muscle atrophy and that specific therapeutic agents may be necessary to combat the atrophy seen under different conditions.
Publication Title
Distinct protein degradation profiles are induced by different disuse models of skeletal muscle atrophy.
Sample Metadata Fields
Sex, Specimen part, Treatment, Time
View Samples- Mus musculus, Homo sapiens
- 56 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Anchorage-independent cell growth signature identifies tumors with metastatic potential.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 26 Downloadable Samples
Description
Cultured cancer cells exhibit substantial phenotypic heterogeneity when measured in a variety of ways such as sensitivity to drugs or the capacity to grow under various conditions. Among these, the ability to exhibit anchorage-independent cell growth (colony forming capacity in semisolid media) has been considered to be fundamental in cancer biology because it has been connected with tumor cell aggressiveness in vivo such as tumorigenic and metastatic potentials, and also utilized as a marker for in vitro transformation. Although multiple genetic factors for anchorage-independence have been identified, the molecular basis for this capacity is still largely unknown. To investigate the molecular mechanisms underlying anchorage-independent cell growth, we have used genome-wide DNA microarray studies to develop an expression signature associated with this phenotype. Using this signature, we identify a program of activated mitochondrial biogenesis associated with the phenotype of anchorage-independent growth and importantly, we demonstrate that this phenotype predicts potential for metastasis in primary breast and lung tumors.
Publication Title
Anchorage-independent cell growth signature identifies tumors with metastatic potential.
Sample Metadata Fields
No sample metadata fields
View Samples