The comparison of trancriptomes was part of the study by Pasternak et al. The goal was to check if BTG4 regulates mRNA polyadenylation during mouse oocyte meiosis. To test this we compared the abundancies of the polyadenylated trancripts in control and Btg4-depleted oocytes. Overall design: 3 samples of 50 oocytes were collected for both groups
The BTG4 and CAF1 complex prevents the spontaneous activation of eggs by deadenylating maternal mRNAs.
Cell line, Subject
View SamplesThe comparison of trancriptomes was part of the study by Pfender, Kuznetsov, Pasternak et al, titled: "Live imaging RNAi screen reveals genes essential for meiosis in mammalian oocytes". The goal was to check if the oocytes cultured in vitro in follicles (for RNAi studies) correspond to real gametes obtained directly from mice (in vivo). Apart from functional experiments showing that they can be fertilized and develop into an embryo, we also compared transcriptomes of those oocytes. Overall design: 3 samples of 50 oocytes were collected for both groups of in vitro and in vivo grown oocytes.
Live imaging RNAi screen reveals genes essential for meiosis in mammalian oocytes.
No sample metadata fields
View SamplesCirculating microvesicles (MVs) have been described as important players in cell-to-cell communication carrying biological information both in normal and pathologic condition. MVs released by cancer cells may incorporate biomolecules such as active lipids, proteins and RNA, which can be delivered and internalized by recipient cells potentially altering gene expression of receiving cells eventually impacting disease progression. In this study, we took advantage of a leukemia in vitro model to investigate MVs as vehicles of protein coding messages. Leukemic cell lines (K562, REH and SHI-1) carrying recurrent translocations were analyzed. In the leukemic cells these translocations are transcribed into oncogenic fusion transcripts. Here, using gene expression microarrays we monitored leukemic fusion transcripts as hallmarks of leukemic cells transcriptome to track mRNA transfer from parental cells to MVs. Transcriptome analysis of K562 cells and released MVs disclosed MVs as not just small scale cells. In fact, a number of transcripts related to membrane activity, cell surface receptors and extracellular communication were enriched in the MVs pool. On the other hand, sets of transcripts related to the basal cellular functions and transcripts of the BCR-ABL oncogenic pathway downstream of the fusion protein were detected in MVs as well as in parental K562 cells. Moreover, through co-culture analyses uptake of leukemic MVs in receiving cells was confirmed and an MV-dosage dependent increase of target cell proliferation was demonstrated.
Expression Profiling of Circulating Microvesicles Reveals Intercellular Transmission of Oncogenic Pathways.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Specimen part, Disease, Disease stage, Cell line, Treatment
View SamplesA majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease.
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Specimen part, Disease, Disease stage
View SamplesA majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease.
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Specimen part, Disease, Disease stage
View SamplesA majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the impact of chronic exposure to the pro-inflammatory cytokine, interferon gamma, on the growth and barrier functions of the oral epithelium.
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Cell line, Treatment
View SamplesmRNA expression data were collected from patients with brain tumor to improve diagnostic of gliomas on molecular level.
Neuronal and glioma-derived stem cell factor induces angiogenesis within the brain.
No sample metadata fields
View SamplesThe Epidermal Growth Factor Receptor (EGFR)/ligand system is centrally involved in multiple homeostatic functions of the epithelia. Epithelial cells are the primary targets of humanized antibodies and small molecule inhibitors against this system, whereby the constellation of skin-specific side effects of these drugs stems from a profound disturbance of keratinocyte biology. So far, the molecular mechanisms underlying these toxic events have been investigated only broadly. Here we show that keratinocyte response to anti-EGFR drugs comprises the development of a type 1 interferon (IFN) molecular signature including enhanced expression of IFN-kappa. Mechanistically, nuclear accumulation of IRF1 precedes this signature as well as the enhanced expression of a chemokine cluster we previously identified as a relevant pro-inflammatory component of EGFR inhibition. In fact, either silencing of IRF1 transcript expression, or antibody-mediated blockade of type 1 IFN receptor function and consequent abrogation of STAT1 activation, leads to impairment of this gene transcription profile. High levels of IRF1 and IFN-kappa can be clearly observed in the early skin lesions of patients treated with cetuximab. Type 1 IFN signaling could be crucially implicated in the triggering of the inflammatory mechanisms active in the skin of patients under treatment with anti-EGFR drugs.
Epidermal growth factor receptor inhibitors trigger a type I interferon response in human skin.
Specimen part, Cell line
View SamplesWe investigated the occupancy of RNA PolII and INTS11 during the stimulation of EGF and compared with drug treated condition using inhibitors against MAPK pathway and Integrator. Additionally, we examined transcription by sequencing the chromatin-bound fraction of RNA. Overall design: We employed several cel lines in our experiment, including HELA, KRAS mutant lung cancer cell line A549 and BRAF mutatant melanoma cell line A375. The conditons we checked including EGF stimulation, MAPK pathway inhibition using BRAF, MEK or ERK inhibitiors, targeting INTS11 with RNAi or integrator inhibitor. We used RNA sequencing to measure the expression profile and CHIP sequencing to detect INTS11 and RNA PolII recruitment on chromatin.
Integrator orchestrates RAS/ERK1/2 signaling transcriptional programs.
No sample metadata fields
View Samples