This SuperSeries is composed of the SubSeries listed below.
Linking DNA methyltransferases to epigenetic marks and nucleosome structure genome-wide in human tumor cells.
Specimen part, Cell line
View SamplesWe used microarrays to profile gene expression of NCCIT cells to study the link between epigenetic modifications and gene transcription.
Linking DNA methyltransferases to epigenetic marks and nucleosome structure genome-wide in human tumor cells.
Specimen part
View SamplesAbnormal NF-kB2 activation has been reported in several types of human leukemia and lymphomas although the exact mechanisms and affected pathways are not clear. We have investigated these questions through the use of a unique transgenic mouse model with lymphocyte-targeted expression of p80HT, a lymphoma associated NF-kB2 mutant. Microarray analysis, verified at the RNA and protein level identified new downstream targets and confirmed established regulatory networks. 201 genes were significantly changed, with 126 being upregulated and 75 downregulated. Pathway analysis uncovered both known and unknown interactions between factors important in the development of human B cell lymphomas and multiple myeloma, including cyclins D1 and D2, TRAF1, CD27, BIRC5/survivin, IL-15 and IL-10. Critical roles for STAT3 and TNF receptors are highlighted. Six target genes of STAT3 were identified: cyclins D1and D2, IL-10, survivin, IL-21 and Blimp1. Interfering with STAT3 signaling induced apoptosis in multiple myeloma cell lines. Novel pathways for NF-kB2 are proposed that involve IL-10 and other genes in the differentiation of plasma cells, evasion of apoptosis and proliferation. These pathways were verified with publically available human microarrays. Several treatment strategies based on these findings are discussed.
NF-κB2 mutation targets survival, proliferation and differentiation pathways in the pathogenesis of plasma cell tumors.
Specimen part
View SamplesWe induced acute nephritis by single injection of sheep nephrotoxic serum in mice and then treated the mice with prostaglandin E2.
No associated publication
Sex, Specimen part
View SamplesWater and ToxB-infiltrated leaves of sensitive cultivar Katepwa were collected at 0,3,9,14,24,48 hours post infiltration (hpi), total RNA was extracted and processed. Expression levels were obtained using Affymetrix GeneChip Wheat Genome Array
Transcriptional changes induced by Ptr ToxB
Specimen part, Treatment, Time
View SamplesComparison of Total RNA and Polysome-bound RNA populations in deltaTOR containing cells and control cells upon hepatocyitc differentiation.
Mammalian target of rapamycin activation impairs hepatocytic differentiation and targets genes moderating lipid homeostasis and hepatocellular growth.
Specimen part, Cell line
View SamplesComparison of transcriptional and translational regulation upon hepatocytic diffentiation by Total RNA and polysome bound RNA profiling.
Translational control plays a prominent role in the hepatocytic differentiation of HepaRG liver progenitor cells.
Sex, Age, Specimen part, Cell line, Time
View SamplesThe goal of this project is to identify genes preferentially expressed in inflammatory macrophages as compared with control macrophages.
Cutting Edge: IL-36 Receptor Promotes Resolution of Intestinal Damage.
Specimen part, Treatment
View SamplesThe lung is the entry site for Bacillus anthracis in inhalation anthrax, the most deadly form of the disease. Spores must escape through the alveolar epithelial cell (AEC) barrier and migrate to regional lymph nodes, germinate and enter the circulatory system to cause disease. Several mechanisms to explain alveolar escape have been postulated, and all these tacitly involve the AEC barrier. In this study, we incorporate our primary human type I AEC model, microarray gene profiling and gene enrichment analysis to study the response of AEC to B. anthracis, (Sterne) spores at 4 and 24 hours post-exposure. Spore exposure altered gene expression in AEC after 4 and 24 hours and differentially expressed genes (1.3 fold, p 0.05) included CCL4/MIP-1 (4 hours), CXCL8/IL-8 (4 and 24 hours) and CXCL5/ENA-78 (24 hours). Gene enrichment analysis revealed that pathways involving cytokine or chemokine activity, receptor binding, and innate immune responses to infection were prominent. Microarray results were confirmed by qRT-PCR and multiplex ELISA assays. Chemotaxis assays demonstrated that spores induced the release of biologically active neutrophil and monocyte chemokines, and that CXCL8/IL-8 was the major neutrophil chemokine. The small or sub-chemotactic doses of CXCL5/ENA-78, CXCL3/GRO and CCL20/MIP-3 may contribute to chemotaxis by priming effects. These data provide the first whole transcriptomic description of the human type I AEC initial response to B. anthracis spore exposure, and contribute to an increased understanding of the role of AEC in the pathogenesis of inhalational anthrax.
No associated publication
Sex, Specimen part, Race, Subject
View SamplesMB114 cells cultured on Matrigel for 1, 5, 15, 25 hours
No associated publication
No sample metadata fields
View Samples