This SuperSeries is composed of the SubSeries listed below.
Viral microRNA targetome of KSHV-infected primary effusion lymphoma cell lines.
Cell line
View SamplesPrimary effusion lymphoma (PEL) is caused by Kaposi''s sarcoma-associated herpesvirus (KSHV) and frequently also harbors Epstein-Barr virus (EBV). The expression of KSHV- and, often, EBV-encoded microRNAs (miRNAs) in PELs suggests a role for these miRNAs in viral latency and lymphomagenesis. Here we report the direct and transcriptome-wide identification of miRNA target sites for all miRNAs expressed in PEL cell lines. The resulting dataset revealed that KSHV miRNAs directly target more than 2000 cellular mRNAs encoding proteins that function in pathways with relevance to KSHV pathogenesis. Moreover, ~50% of these mRNAs are also targeted by EBV miRNAs, via distinct binding sites. In addition to a known viral analog of miR-155, we show that KSHV encodes a viral miRNA that mimics cellular miR-142-3p function. In summary, these experiments identify an extensive list of mRNAs targeted by KSHV miRNAs and indicate that these are likely to strongly influence viral replication and pathogenesis. Overall design: small RNA sequencing, 3 samples Ago2 (EIF2C2) PAR-CLIP, 2 samples
Viral microRNA targetome of KSHV-infected primary effusion lymphoma cell lines.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesResponse of A549 cells treated with Aspergillus fumigatus wild type germinating conidia (WT_GC) or PrtT protease deficient mutant conidia (PrtT-GC) or inert acrylic 2-4 micron beads (Beads) for 8h
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesResponse of A549 cells treated with Aspergillus fumigatus wild type culture filtrate (WT-CF) or PrtT protease deficient mutant culture filtrate (PrtT-CF) for 8h
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesResponse of A549 cells treated with Aspergillus fumigatus germinating conidia (WT-GC) or culture filtrate (WT-CF) for 8h
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesMicroarrays were used to examine gene expression changes that may be present in the fallopian tube epithelium of morphologically normal BRCA1 mutation positive and negative subjects. Fallopian tube epithelia has been implicated as an early point of origin for serous carcninoma. By examining the early events present in the microenvironment of this tissue between BRCA1 mutation carriers and non-carriers, we hoped to elucidate mechanisms that may lead to the development of epithelial ovarian cancer.
Identification of abrogated pathways in fallopian tube epithelium from BRCA1 mutation carriers.
Specimen part
View SamplesThe cellular response to DNA damage is vital for maintaining genomic stability and preventing undue cell death or cancer formation. The DNA damage response (DDR), most robustly mobilized by double-strand breaks (DSBs), rapidly activates an extensive signaling network that affects numerous cellular systems, leading to cell survival or programmed cell death. A major component of the DDR is the widespread modulation of gene expression. We analyzed transcriptional responses to ionizing radiation (IR) in 5 human cell lines to elucidate the scope of this response and identify its gene targets. According to the mRNA expression profiles most of the responses were cell line-specific. Data analysis identified significant enrichment for p53 target genes and cell cycle-related pathways among groups of up-regulated and down-regulated genes, respectively.
Transcriptional modulation induced by ionizing radiation: p53 remains a central player.
Cell line, Time
View SamplesFive degradome libraries were constructed from three different seed developmental stages. Separate degradome libraries were constructed for seed coat and cotyledons to identify the tissue specific miRNAs and their potential targets. Sequencing and analysis of degradome libraries gives identification of 183 different targets for 80 known soybean miRNAs. We found 30 cotyledon specific, 18 seed coat specific and 32 miRNAs found in both tissues irrespective of the developmental stages. One interesting observation is that we found more miRNA targets in late seed developmental stages than earlier stages. Additionally, we have validated four different auxin response factor genes as targets for gma-miR160 via RNA ligase mediated 5' rapid amplification of cDNA ends (RLM-5'RACE). GO analysis indicated the enrichment of miRNA target genes in seed development. Overall design: Construction of degradome libraries using cotyledons and seed coats from 3 different developmental stages
Identification of soybean seed developmental stage-specific and tissue-specific miRNA targets by degradome sequencing.
Specimen part, Subject
View SamplesCell migration is central to many biological processes including embryonic development, wound healing, and cancer progression. Cell migration is sensitive to environmental stiffness, and many cell types exhibit a stiffness optimum at which migration is maximal. Here we present a cell migration simulator that predicts a stiffness optimum that can be shifted by altering the number of active molecular motors and clutches. This prediction is verified experimentally by comparing cell traction and F-actin retrograde flow for two cell types with differing amounts of active motors and clutches: embryonic chick forebrain neurons (ECFNs; optimum ~1 kPa) and U251 glioma cells (optimum ~100 kPa). In addition, the model predicts, and experiments confirm, that the stiffness optimum of U251 glioma cell migration, morphology, and F-actin retrograde flow rate can be shifted to lower stiffness by simultaneous drug inhibition of myosin II motors and integrin-mediated adhesions.
Shifting the optimal stiffness for cell migration.
Sex, Cell line
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