Significance of RNA methylation in the context of HIV-1 infection in human T cells Overall design: MeRIP-Seq of Control and HIV-infected MT4 T-Cells
Dynamics of the human and viral m(6)A RNA methylomes during HIV-1 infection of T cells.
No sample metadata fields
View SamplesWe have analyzed 2 normal B cells isolated from peripheral blood and 5 CLL specimens with affy 133A microarray for expression.
Aberrant splicing of the E-cadherin transcript is a novel mechanism of gene silencing in chronic lymphocytic leukemia cells.
Specimen part, Disease, Disease stage
View SamplesPU.1 is a key transcription factor for macrophage differentiation. Novel PU.1 target genes were identified by mRNA profiling of PU.1-deficient progenitor cells (PUER) before and after PU.1 activation. We used two different types of Affymetrix DNA-microarrays (430 2.0 arrays and ST 1.0 exon arrays) to characterize the global PU.1-regulated transcriptional program underlying the early processes of macrophage differentiation.
Transcriptomic profiling identifies a PU.1 regulatory network in macrophages.
No sample metadata fields
View SamplesMecp2 loss-of-function has been associated with altered gene expression in many tissues. We characterized gene expression changes within the hippocampi of 3 different Mecp2 loss-of-function mouse models.
An AT-hook domain in MeCP2 determines the clinical course of Rett syndrome and related disorders.
Age, Specimen part
View SamplesSilver nanoparticles are used in consumer products like food contact materials, drinking water technologies and supplements, due to their antimicrobial properties. This leads to an oral uptake and exposure of intestinal cells. In contrast to other studies we found no apoptosis induction by surfactant coated silver nanoparticles in the intestinal cell model Caco-2 in a previous study, although the particles induced oxidative stress, morphological changes and cell death. Therefore, this study aimed to analyze the molecular mechanism of silver nanoparticles in Caco-2 cells. We used global gene expression profiling in differentiated Caco-2 cells, supported by verification of the microarray data by quantitative real time RT-PCR and microscopic analysis, impedance measurements and assays for apoptosis and oxidative stress. Our results revealed that the majority of surfactant coated silver nanoparticles are not taken up into differentiated Caco-2 cells. and probably affect the cells by outside-in signaling. They induce oxidative stress and have an influence on canonical pathways related to FAK, ILK, ERK, MAPK, integrins and adherence and tight junctions, thereby inducing transcription factors like AP1, NFB and NRF2, which mediate cellular reactions in response to oxidative stress and metal ions and induce changes in the cytoskeleton and cell-cell and cell-matrix contacts. The present data confirm the absence of apoptotic cell death. Non-apoptotic, necrotic cell death, especially in the intestine, can cause inflammation and influence the mucosal immune response.
Molecular mechanism of silver nanoparticles in human intestinal cells.
Cell line
View SamplesThe data shows the effect of NMD inhbition on cell lines and the change in RNA transcripts. The data also shows comparison of non-transformed cells (tert kert) to a Head and Neck tumorigenic cell line SCC12.
Exon 11 skipping of E-cadherin RNA downregulates its expression in head and neck cancer cells.
Specimen part
View SamplesThe specification of hematopoietic cells in the developing embryo occurs in specific stages and is regulated by the successive establishment of specific transcriptional networks. However, the molecular mechanisms of how the different stages switch from one to another are still not well understood. Hematopoietic cells arise from endothelial cells within the dorsal aorta which transit into hematopoietic cells by a process called the endothelial-hematopoietic transition (EHT) which does not involve DNA replication. The transcription factor RUNX1 is essential for this process. Using the differentiation of mouse embryonic stem cells carrying an inducible version of RUNX1, we have previously shown that hematopoietic genes are primed prior to the EHT by the binding of transcription factors required to form both endothelial and hematopoietic cells (FLI-1 and SCL/TAL1). We demonstrated that after induction RUNX1 reshapes the transcription factor binding landscape by causing a relocation of these factors and pulling them towards its binding sites. In the study presented here, we employed the same system to globally dissect the transcriptional processes that underlay the EHT. We demonstrate that the RUNX1-mediated movement of FLI-1 involves the recruitment of the basal transcription components CDK9 and BRD4 to promoters. The looping factor LDB1 to binds to distal elements and after induction relocates towards RUNX1/FLI-1 to form a co-localizing complex in chromatin. This entire process is blocked by treatment with the BRD4 inhibitor JQ1. Our study constitutes a paradigm for transcriptional processes driving transitions in cellular shape and function which are widely observed in development and disease. Overall design: RNA-seq expreiments have been used to study RUNX1 transcription factor during Hematopoietic specification
The Co-operation of RUNX1 with LDB1, CDK9 and BRD4 Drives Transcription Factor Complex Relocation During Haematopoietic Specification.
Specimen part, Subject
View SamplesExtrarenal viral infections commonly trigger glomerulonephritis mostly in association with immune complex disease. The immunoglobulin component of immune complexes can activate glomerular cell Fc receptors but whether complexed viral nucleic acids contribute to glomerular inflammation remains unknown. Glomerular mesangial cells express TLR3 but lack TLR7-9, hence, it is unclear whether mesangial cells can recognize and respond to viral ssRNA or DNA. Here we studied the immune responses activated by 3P-RNA (5'Triphosphate RNA) and Non-CpG DNA (Double stranded DNA) in primary mesangial cells (PMC).
Viral RNA and DNA trigger common antiviral responses in mesangial cells.
No sample metadata fields
View SamplesThe Wnt/alpha-catenin pathway plays a central role in epidermal homeostasis and regeneration but how it affects fibroblast fate decisions is unknown. Here, we investigated the effect of targeted alpha-catenin stabilization in dermal fibroblasts. Comparative gene expression profiling of Sca1- and Sca1+ neonatal fibroblasts, from upper and lower dermis respectively, confirmed that Sca1+ cells had a pre-adipocyte signature and revealed differential expression of Wnt/alphacatenin-associated genes. By targeting all fibroblasts or selectively targeting Dlk1+ lower dermal fibroblasts, we found that -catenin stabilization between E16.5 and P2 resulted in a reduction in the dermal adipocyte layer with a corresponding increase in dermal fibrosis and an altered hair cycle. The fibrotic phenotype correlated with a reduction in the potential of Sca1+ fibroblasts to undergo adipogenic differentiation ex vivo. Our findings indicate that Wnt/alpha-catenin signaling controls adipogenic cell fate within the lower dermis, which potentially contributes to the pathogenesis of fibrotic skin diseases.
β-Catenin Stabilization in Skin Fibroblasts Causes Fibrotic Lesions by Preventing Adipocyte Differentiation of the Reticular Dermis.
Specimen part
View SamplesThe goals of this study are to utilize high-throughput transcriptome sequencing of mutant and control fetal testis samples to identify changes in both transcript and repeat element abundance in tissues harboring a homozygous mutation for Glis3. 672 unique genes were differentially expressed in mutant versus wild-type samples. Of the downregulated genes, there was a strong enrichment for piRNA pathway members, while upregulated genes were associated with leydig cell differentiation, meiosis, and histone cluster genes. Differential expression of several repeat elements was also detected in mutant samples. Our findings provide valuable information on the potential mechanisms underlying the fetal germ cell loss observed in Glis3 mutant testes. Overall design: Whole testis mRNA profiles of embryonic day 14.5 wild type (WT) and Glis3 mutant mice were generated by deep sequencing, using Illumina HiSeq2500
Loss of Glis3 causes dysregulation of retrotransposon silencing and germ cell demise in fetal mouse testis.
Specimen part, Subject
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