Gene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing the zinc transporter ZIP8 (SLC39A8) protein.
Pleiotropic roles of metallothioneins as regulators of chondrocyte apoptosis and catabolic and anabolic pathways during osteoarthritis pathogenesis.
Age, Specimen part, Treatment
View SamplesGene expression profiling of primary mouse articular chondrocyte treated with interleukin-1.
Estrogen-related receptor γ causes osteoarthritis by upregulating extracellular matrix-degrading enzymes.
Age, Specimen part, Treatment
View SamplesTo gain further insight into the biological effects of JH4, we investigated its impact on gene expression profiles.
Interruption of progerin-lamin A/C binding ameliorates Hutchinson-Gilford progeria syndrome phenotype.
Sex, Specimen part, Disease
View SamplesThe Drosophila phagocytic receptor Eater is expressed specifically in phagocytic hemocytes. It contributes to host immune defense and is required for survival of bacterial infections. Eater is involved in recognition and phagocytosis of bacteria.
Phagocytosis of bacterial pathogens.
Cell line, Treatment, Time
View SamplesAnalysis between two different types of T cells
Comparison of Invariant NKT Cells with Conventional T Cells by Using Gene Set Enrichment Analysis (GSEA).
Sex, Specimen part
View SamplesStevens-Johnson syndrome (SJS) and toxic epidermal necrolysis
Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis.
No sample metadata fields
View SamplesStevens-Johnson syndrome (SJS) and toxic epidermal necrolysis
Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis.
No sample metadata fields
View SamplesWe found that RANKL, expressed by cancer cells or derived from exogenous sources, consistently induced human prostate, breast, kidney, lung and liver cancer cells to colonize or metastasize to bone in an animal model of cancer bone metastasis. RANK-mediated signaling established a premetastatic niche through a forward feedback loop by inducing RANKL and c-Met expression and downstream signaling via upregulation of master regulator transcription factors regulating EMT (Twist1, Slug, Zeb1, Zeb2), stem cells (Sox2, Myc, Oct3/4 and Nanog), neuroendocrine cells (Sox 9, HIF-1 and FoxA2) and osteomimicry (c-Myc/Max, Sox2, Sox9, HIF1 and Runx2). Abrogating RANK or its downstream signaling network, c-Myc/Max or c-Met, abolished PCa skeletal metastasis in mice. We observed that a small number of RANKL-expressing PCa cells can initiate bone and soft tissue metastases by recruiting non-tumorigenic or bystander PCa or host cells from the circulation or at metastatic sites to co-colonize bone. The recruited bystander PCa cells assume the phenotypes of RANKL-expressing PCa cells by expressing increased c-Met, phosphorylated c-Met and RANKL. RANKL expression at a single cell level in primary PCa tissues predicted disease-specific survival, reflecting the significant role of RANKL-RANK signaling in the development of lethal bone metastasis.
RANK- and c-Met-mediated signal network promotes prostate cancer metastatic colonization.
Specimen part, Cell line
View SamplesComparative analysis of mouse cardiac left ventricle gene expression: voluntary wheel exercise and pregnancy-induced cardiac hypertrophy
Distinct cardiac transcriptional profiles defining pregnancy and exercise.
Sex, Specimen part
View SamplesThe placenta is an understudied organ that has a critical role in mammalian development. In early placental development, the essential process of trophoblast invasion establishes adequate blood flow between mother and fetus. Despite its importance, little is known about the genomic regions responsible for regulating trophoblast invasion. In order to identify enhancers that are important for regulating the process, we carried out ChIP-Seq for an enhancer-associated mark at two time points during early placental development. Combining these data with RNA-Seq data and protein interaction data allowed us to construct a gene-enhancer network describing trophoblast invasion. Overall design: RNA-Seq at two time points in early placenta development (e7.5 an e9.5). There are 3 biological replicates per time point. Samples were pooled and sequenced on two lanes.
Changes in the enhancer landscape during early placental development uncover a trophoblast invasion gene-enhancer network.
No sample metadata fields
View Samples