We performed a 3' RACE of a novel HIV RNA TAR-gag in order to determine the sequence of the RNA at the 3' end. Our data had shown that TAR-gag was potentially a noncoding RNA and our hypothesis was that TAR-gag ended somewhere prior to the end of the gag region of the HIV genome. The 3' RACE experiment showed that TAR-gag actually consists of four different RNA clusters, the longest of which ends at 615 bases from the transcription start site; this is in the middle of the p17 region of the gag gene. In addition, we sequenced all host RNAs in the EVs. Overall design: RNA from J1.1 and U1 exosomes was isolated and converted to cDNA. Sequencing libraries of the cDNA were made and a 3' RACE was perforemed to determine how long TAR-gag RNA is. Please note that the clustering analysis (published in PMID 28536264) was done only on the unfragmented samples (i.e. *-U samples).
An Omics Approach to Extracellular Vesicles from HIV-1 Infected Cells.
Specimen part, Subject
View SamplesGene expression signatures have the capacity to identify clinically significant features of breast cancer and can predict which individual patients are likely to be resistant to neoadjuvant therapy, thus providing the opportunity to guide treatment decisions.
Gene expression profiles of multiple breast cancer phenotypes and response to neoadjuvant chemotherapy.
Specimen part
View SamplesSkeletal muscle regeneration is a highly dynamics process. The study aims at investigating gene expression by endothelial cells and satellite/myogenic cells during this process, in mouse, after a toxic injury
Coupling between Myogenesis and Angiogenesis during Skeletal Muscle Regeneration Is Stimulated by Restorative Macrophages.
Specimen part, Time
View SamplesComparison between cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel
Transcript and protein expression profiles of the NCI-60 cancer cell panel: an integromic microarray study.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesTh17 cells were sorted ex vivo from PB of healthy donors as CD4+CD161+CCR6+CXCR3-. Following, cells were transduced with a lentiviral vector carrying the Eomes gene or with an empty vector. Infected cells were then enriched by MACS separation using the reporter gene NGFR as selection marker. Finally, cells were frozen for RNA analysis.
Eomes controls the development of Th17-derived (non-classic) Th1 cells during chronic inflammation.
Cell line
View SamplesHuman adenovirus 5 encodes a small set of miRNAs, which are generated by DICER-mediated processing of 2 larger precursors, the so-called virus-associated RNAs I and II. To identify targets of one of the major miRNA isoforms derived from virus-associated RNAI (mivaRNAI-137), we isolated Argonaute complexes of mivaRNAI-137-transfected cells and analyzed co-purifying RNAs by microarray analysis. RNAs enriched in Argonaute complexes of mivaRNAI-137-transfected cells compared to cells transfected with a control siRNA were identified and subjected to further validation. RNAs specifically associated with Argonaute-containining complexes of adenovirus 5-infected cells were identified as well.
Identification of RISC-associated adenoviral microRNAs, a subset of their direct targets, and global changes in the targetome upon lytic adenovirus 5 infection.
Cell line
View SamplesEach total RNA sample is hybridized to two different arrays: Affymetrix U133A (GPL96) and U133B (GPL97).
Previously unidentified changes in renal cell carcinoma gene expression identified by parametric analysis of microarray data.
No sample metadata fields
View SamplesTo understand the transcriptional program controlled by AGL24, we took advantage of a functional estradiol-inducible AGL24 expression system in combination with microarray analysis to identify AGL24 target genes.
Direct interaction of AGL24 and SOC1 integrates flowering signals in Arabidopsis.
No sample metadata fields
View SamplesThe neurobiological functions of a number of kinases expressed in the brain are unknown. Here, we report new findings on DCLK3 (Doublecortin-like kinase 3) which is preferentially expressed in neurons in the striatum and dentate gyrus. Its function has never been investigated. DCLK3 expression is markedly reduced in Huntington''s disease. Recent data obtained in studies related to cancer suggest DCLK3 could have anti-apoptotic effect. Thus, we hypothesized that early loss of DCLK3 in Huntington''s disease may render striatal neurons more susceptible to mutant huntingtin (mHtt). We discovered that DCLK3 silencing in the striatum of mice exacerbated the toxicity of an N-terminal fragment of mHtt. Conversely, overexpression of DCLK3 reduced neurodegeneration produced by mHtt. DCLK3 also produced beneficial effects on motor symptoms in a knock-in mouse model of Huntington''s disease. Using different mutants of DCLK3, we found that the kinase activity of the protein plays a key role in neuroprotection. To investigate the potential mechanisms underlying DCLK3 effects, we studied the transcriptional changes produced by the kinase domain in human striatal neurons in culture. Results show that DCLK3 regulates in a kinase-dependent manner the expression of many genes involved in transcription regulation and nucleosome/chromatin remodeling. Consistent with this, histological evaluation showed DCLK3 is present in the nucleus of striatal neurons and, protein-protein interaction experiments suggested that the kinase domain interacts with zinc finger proteins, including TADA3, a core component of SAGA complex. Our novel findings suggest that the presence of DCLK3 in striatal neurons may play a key role in transcription regulation and chromatin remodeling in these brain cells, and show that reduced expression of the kinase in Huntington's disease could render the striatum highly vulnerable to neurodegeneration. Examination of DCLK3 as neuroprotector against mutant huntingtin in vivo and in vitro models. Overall design: Examination of DCLK3 as neuroprotector against mutant huntingtin in vitro experiments.
The striatal kinase DCLK3 produces neuroprotection against mutant huntingtin.
Specimen part, Cell line, Subject
View SamplesDisseminated prostate cancer cells colonize the skeleton to progress into macroscopic lesions only if they successfully adapt to the bone microenvironment. We previously reported that the ability of prostate cancer cells to generate skeletal tumors in animal models correlated with the expression of the alpha-receptor for Platelet-Derived Growth Factor (PDGFRa). In this study we aimed to identify PDGFRa-regulated genes responsible for the acquisition of a bone-metastatic prostate phenotype. We performed genome-wide expression comparative analyses of human prostate cancer cell lines that differ for PDGFRa expression and propensity to establish tumors in the skeleton of animal models. We investigated the genes that were differentially regulated in the highly bone-metastatic PC3-ML cells and their low-metastatic counterpart PC3-N cells, and the genes differentially regulated between PC3-N and PC3-N with overexpression of PDGFRa (PC3NRa). We have previously shown that DU-145 cells lack PDGFRa and fail to survive longer than three days as disseminated tumor cells after homing to the mouse bone marrow. Interestingly, and in contrast to PC3-N cells, the exogenous expression of PDGFRa did not promote metastatic bone-tropism of DU-145 cells in our model. Thus, we examined the genes that were differentially regulated between DU-145 and DU-145(Ra) and excluded them from our candidate genes. Finally, to refine our findings and compensate for PC3 and DU-145 genetic disparity, we performed a comparative analysis of the genes differentially regulated between two bone metastatic single-cell progenies that were derived from PC3-ML cells.
Interleukin-1β promotes skeletal colonization and progression of metastatic prostate cancer cells with neuroendocrine features.
Cell line
View Samples