DPRP (PRL8a2) is critically involved in adaptations of the placentation site to physiological stressors. DPRP (PRL8a2) restrains the expression of genes associated with ER stress.
Identification of target genes for a prolactin family paralog in mouse decidua.
Specimen part
View SamplesRNA-seq data demonstrate that N1 plus R848 at the global gene expression level synergistically promotes DC maturation and subsequent upregulation of many genes in DCs that are involved in the polarization of CD4+ T cells into Th1-type effectors. Overall design: DCs sham-treated or treated with N1, R848, or N1 plus R848 for 4 hours.
HMGN1 and R848 Synergistically Activate Dendritic Cells Using Multiple Signaling Pathways.
Specimen part, Treatment, Subject
View SamplesWe synthesized the PAX8-NFE2L2 fusion transcript and cloned it into a lentiviral vector, and used this to overexpress it in the murine prostate adenocarcinoma cell line TRAMP-C1. Overall design: We used high coverage RNA sequencing (>30 million reads per sample) to compare the expression profiles of cells expressing the PAX8-NFE2L2 fusion transcript to cells transduced with an empty vector.
Global analysis of somatic structural genomic alterations and their impact on gene expression in diverse human cancers.
Specimen part, Cell line, Subject
View SamplesColorectal cancer cells with TP53 mutation are highly resistant to chemotherapeutics. In order to identify potential chemo-resistance signatures, here; we explored the global gene expression profiles of drug resistant colorectal cancer cell line SW480 upon Floxuridine (FdUrd) treatment using Illumina Human HT-12 v4.0 Expression Beadchip Array. Further, significantly altered genes were subjected to the pathway analysis in GeneCodis3 and crucial signaling pathways were found to be enriched. Upon further functional validations, these pathways could be targeted to enhance therapy in human cancers harboring mutant p53.
Transcriptome profiling identifies genes and pathways deregulated upon floxuridine treatment in colorectal cancer cells harboring GOF mutant p53.
Sex, Age, Specimen part, Cell line, Treatment
View SamplesWe used microarrays to detail the global program of gene expression underlying identified distinct classes of up-regulated or down-regulated genes in salivary glands between Nfkbiz-/- and wild type mice.
Association of a dysbiotic oral microbiota with the development of focal lymphocytic sialadenitis in IκB-ζ-deficient mice.
Sex, Specimen part
View SamplesNiemann-Pick Type C (NPC) disease is a rare, genetic, lysosomal disorder with progressive neurodegeneration. Poor understanding of the pathophysiology and lack of blood-based diagnostic markers are major hurdles in the treatment and management of NPC and several additional neurological, lysosomal disorders. To identify disease severity correlates, we undertook whole genome expression profiling of sentinel organs, brain, liver, and spleen of Balb/c Npc1-/- mice (Npc1nih)relative to Npc1+/- at an asymptomatic stage, as well as early- and late-symptomatic stages. Unexpectedly, we found prominent up regulation of innate immunity genes with age-dependent change in their expression, in all three organs. We shortlisted a set of 12 secretory genes whose expression steadily increased with age in both brain and liver, as potential plasma correlates for the neurological disease. Ten were innate immune genes with eight ascribed to lysosomes. Several are known to be elevated in diseased organs of murine models of other lysosomal diseases including Gauchers disease, Sandhoff disease and MPSIIIB. We validated the top candidate lysozyme, in the plasma of Npc1-/- as well as Balb/c Npc1nmf164 mice (bearing a point mutation closer to human disease mutants) and show its reduction in response to an emerging therapeutic. We further established elevation of innate immunity in Npc1-/- mice through multiple functional assays including inhibition of bacterial infection as well as cellular analysis and immunohistochemistry.
Genomic expression analyses reveal lysosomal, innate immunity proteins, as disease correlates in murine models of a lysosomal storage disorder.
Age, Specimen part, Subject
View SamplesBone mineral density and structure candidate gene analysis in alcohol-non-preferring (NP), alcohol-preferring (P), congenic NP (NP.P) and congenic P (P.NP) rats
Identification of genes influencing skeletal phenotypes in congenic P/NP rats.
No sample metadata fields
View SamplesExpression profiling of proliferating primary myoblasts obtained from vastus lateralis muscle biopsises from healthy individuals and stimulated with Vitamin D (100 nM 1,25(OH)2D3) or vehicle for 24h.
Evidence for Vitamin D Receptor Expression and Direct Effects of 1α,25(OH)2D3 in Human Skeletal Muscle Precursor Cells.
Specimen part, Treatment, Subject
View SamplesThe tumor microenvironment is characterized by low glucose and hypoxia. It is well known that changes in the tumor microenvironment, such as hypoxia and low glucose, can increase the production of VEGF. Although the role of hypoxia in the regulation of VEGF production is well understood, the mechanism linking glucose deprivation (GD) to tumor growth and angiogenesis is unclear. Here, GD (a physiological stimulus) was used to treat human tumor cells. The transcriptional reprogramming of tumor cells by GD was measured with microarray technology to provide a comprehensive analysis of the gene expression profile underlying the GD treatment. Our study suggested that GD initiates an angiogenic switch by increasing the expression of proangiogenic mediators (VEGF, FGF2, IL6, etc.) and decreasing the expression of angiogenesis inhibitors (THBS1, CXCL14 and CXCL10). The markers of Unfolded Protein Response (UPR) (Grp78/Bip, CHOP, ATF4, etc.) were significantly increased. The above results suggest GD may regulate angiogenesis through activation of the UPR.
The unfolded protein response induces the angiogenic switch in human tumor cells through the PERK/ATF4 pathway.
Specimen part, Cell line, Treatment
View SamplesFemoral neck bone mineral density and structure candidate gene analysis in Fischer 344 (F344) and Lewis (LEW) rats
Genomic expression analysis of rat chromosome 4 for skeletal traits at femoral neck.
No sample metadata fields
View Samples