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Mus musculus
18 Downloadable Samples
Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
The lipocalin Apolipoprotein D (ApoD), known to protect the nervous system against oxidative stress (OS) in model organisms, is up-regulated early in the mouse brain in response to the ROS generator paraquat (PQ). However, the processes triggered by this up-regulation have not been explored.
Publication Title
Apolipoprotein D alters the early transcriptional response to oxidative stress in the adult cerebellum.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
We used human gene expression microarray to interrogate how glutamine deprivation differentially impact gene expession in isogenic PIK3CA mutant and WT cells.
Publication Title
5-Fluorouracil Enhances the Antitumor Activity of the Glutaminase Inhibitor CB-839 against <i>PIK3CA</i>-Mutant Colorectal Cancers.
Sample Metadata Fields
Specimen part, Cell line, Treatment
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GSE68169- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
A detailed knowledge of the mechanisms underlying brain aging is fundamental to understand its functional decline and the baseline upon which brain pathologies superimpose. Endogenous protective mechanisms must contribute to the adaptability and plasticity still present in the healthy aged brain. Apolipoprotein D (ApoD) is one of the few genes with a consistent and evolutionarily conserved up-regulation in the aged brain. ApoD protecting roles upon stress or injury are well known, but a study of the effects of ApoD expression in the normal aging process is still missing. Using an ApoD-knockout mouse we analyze the effects of ApoD on factors contributing to the functional maintenance of the aged brain. We focused our cellular and molecular analyses in cortex and hippocampus at an age representing the onset of senescence where mortality risks are below 25%, avoiding bias towards long-lived animals. Lack of ApoD causes a prematurely aged brain without altering lifespan. Age-dependent hyperkinesia and memory deficits are accompanied by differential molecular effects in cortex and hippocampus. Transcriptome analyses reveal distinct effects of ApoD loss on the molecular age-dependent patterns of cortex and hippocampus, with different cell-type contributions to age-regulated gene expression. Markers of glial reactivity, proteostasis, and oxidative and inflammatory damage reveal early signs of aging and enhanced brain deterioration in the ApoD-knockout brain. The lack of ApoD results in an age-enhanced significant reduction in neuronal calcium-dependent functionality markers and signs of early reduction of neuronal numbers in the cortex, thus impinging upon parameters clearly differentiating neurodegenerative conditions from healthy brain aging. Our data support the hypothesis that the physiological increased brain expression of ApoD represents a homeostatic anti-aging mechanism.
Publication Title
Aging without Apolipoprotein D: Molecular and cellular modifications in the hippocampus and cortex.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Rattus norvegicus
- 24 Downloadable Samples
- Affymetrix Rat Expression 230A Array (rae230a)
Description
Gene expression profiles were examined in whole lung tissue collected from male and female Long-Evans rats at different time points after inoculation with Seoul virus (i.e., the species-specific hantavirus that infects Norway rats)
Publication Title
Sex differences in the recognition of and innate antiviral responses to Seoul virus in Norway rats.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina humanRef-8 v2.0 expression beadchip
Description
CD133 (Prominin1) is pentaspan transmembrane glycoprotein expressed in several stem cell populations and cancers. Reactivity with an antibody (AC133) to a glycoslyated form of CD133 has been widely used for the enrichment of cells with tumor initiating activity in xenograph transplantation assays. We have found by fluorescence-activated cell sorting that increased AC133 reactivity in human embryonic stem cells, colon cancer and melanoma cells is correlated with increased DNA content and reciprocally, that the least reactive cells are in the G1/G0 portion of the cell cycle. Continued cultivation of cells sorted on the basis of high and low AC133 reactivity results in a normalization of the cell reactivity profiles indicating that cells with low AC133 reactivity can generate highly reactive cells as they resume proliferation. The association of AC133 with actively cycling cells may contribute to the basis for enrichment for tumor initiating activity.
Publication Title
Cell cycle-dependent variation of a CD133 epitope in human embryonic stem cell, colon cancer, and melanoma cell lines.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
The objective of this study was to identify transcriptional changes differentially regulated by GDF11 stimulation compared to TGFB1
Publication Title
Tumor-Suppressor Inactivation of GDF11 Occurs by Precursor Sequestration in Triple-Negative Breast Cancer.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 1 Downloadable Sample
IlluminaGenomeAnalyzer
Description
Combining an in vitro hNCC differentiation protocol with epigenomic profiling, we provide the first whole-genome characterization of cis-regulatory elements in this highly relevant cell type. With this data at hand, we have characterized the chromatin state and dynamics of all human gene promoters during the course of NCC in vitro differentiation. Most importantly, we have identified a large cohort of active and NCC-specific enhancers, which we showed to be functionally relevant in vivo, in the context of embryonic development. Finally, through sequence analysis of the identified NCC enhancers, we uncovered the orphan nuclear receptors NR2F1 and NR2F2 as novel hNCC transcriptional regulators both in vitro and in vivo. Overall design: RNA-seq experiments in human neural crest cells (hNCC)
Publication Title
Epigenomic annotation of enhancers predicts transcriptional regulators of human neural crest.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 15 Downloadable Samples
- Illumina HiSeq 1000
Description
Specific deletion of suppressor of cytokine signaling 3 (Socs3) in keratinocytes can cause severe skin inflammation with infiltration of immune cells, however the molecular mechanisms and key regulatory pathways involved remains poorly understood. To investigate the role of Socs3 in keratinocytes, we generated and analyzed global RNA-Seq profiles in Socs3 conditional knockout (cKO) mice at two different stages (2- and 10- weeks). Over 400 shared genes were found to be significantly regulated at both time points. Two week samples were marked by initial skin barrier dysfunction established by the downregulation of keratin associated genes and upregulation of genes regulating lipid metabolism. Subsequent increase in expression level of multiple chemokines and cytokines at 10 week were observed representing response to skin inflammation caused by the disruption of skin barrier function. A group of activator protein-1 related genes were to found to be highly elevated in Socs3 cKO mice at both time points. This observation was duly validated using qRT-PCR in Socs3 depleted human keratinocyte–derived HaCaT cells. Overall this study reveals an important regulatory dynamics of Socs3 in skin barrier dysfunction. Overall design: Socs3 cKO mice mRNA profiles of 2 and 10 week wild type (WT) C57BL/6 mice were generated by sequencing using HiSeq 1000 system (Illumina) machine which could read a 50 bp sequence.
Publication Title
Insights into gene expression profiles induced by Socs3 depletion in keratinocytes.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 68 Downloadable Samples
Illumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Immunodeficiency, autoinflammation and amylopectinosis in humans with inherited HOIL-1 and LUBAC deficiency.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject, Time
View Samples- Homo sapiens
- 9 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip
Description
HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF- and IL-1 on transcriptional changes of primary fibroblasts from HOIL-1-, MYD88- and NEMO-deficient patients.
Publication Title
Immunodeficiency, autoinflammation and amylopectinosis in humans with inherited HOIL-1 and LUBAC deficiency.
Sample Metadata Fields
Disease, Disease stage, Subject, Time
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