We report a new protein complex with a role in transcription elongation that is formed by Ypr045c (Thp3) and the Csn12 component of the COP9-signalosome. Thp3-Csn12 is recruited to transcribed genes. Their mutations suppress the gene expression defects of mutants of the THO complex involved in mRNP biogenesis and export and show defects in mRNA accumulation. In vivo transcription elongation impairment of thp3 mutants is shown by reduction of RNAPII recruitment throughout an active gene and in transcript run on analysis performed in G-less systems. This new complex establishes a novel link between transcription and mRNA processing.
New suppressors of THO mutations identify Thp3 (Ypr045c)-Csn12 as a protein complex involved in transcription elongation.
No sample metadata fields
View SamplesCompares shFOXO4 vs. Control in LNCaP grown in culture, or in nude mice as primary orthotopic tumors or lymph node metastases
A genome-wide RNAi screen identifies FOXO4 as a metastasis-suppressor through counteracting PI3K/AKT signal pathway in prostate cancer.
Specimen part
View SamplesPrimary skin fibroblasts from HGPS patients and an age-matched control wild-type individuals were challenged in a standard transformation assay by retroviral introduction of TERT (T), V12-HRAS (R) and SV40 large and small T antigens (S). TERT-Immortalized cell lines from the same sources were also generated.
Transformation resistance in a premature aging disorder identifies a tumor-protective function of BRD4.
Specimen part
View SamplesBaseline gene expression of adipose stem cell derived iPSCs generated by lentiviral Yamanaka 4 factors. We used microarrays to analyze the global gene expression of hACS derived iPSCs with KMOS and KMOS+miR-302.
MicroRNA-302 increases reprogramming efficiency via repression of NR2F2.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Epigenetic Networks Regulate the Transcriptional Program in Memory and Terminally Differentiated CD8+ T Cells.
Specimen part, Treatment
View SamplesTo elucidate the gene expression footprint of antigenically challenged T-cells which had been treated with anti-LFA-1, CTLA4Ig, anti-CD40-ligand antibodies, we performed microarray gene expression analysis comparing the expression profile of costimulatory blockade treated and untreated responder T-cells.
Short-term immunosuppression promotes engraftment of embryonic and induced pluripotent stem cells.
Specimen part
View SamplesEpigenetic mechanisms play a critical role during differentiation of T cells by contributing to the formation of stable and heritable transcriptional patterns. To further study the mechanisms of memory maintenance in CD8+ T cells, we performed genome-wide analysis of DNA methylation, histone marking (H3K9Ac and H3K9me3) and gene expression profiles in naive, effector memory (EM) and terminally differentiated memory (TEMRA) cells. Our results indicate that DNA demethylation and histone acetylation are coordinated to generate the transcriptional program associated with memory cells. Conversely, EM and TEMRA cells share a very similar epigenetic landscape. Nonetheless, the TEMRA transcriptional program predicts an innate immunity phenotype associated with genes never reported in these cells, including several mediators of NK cell activation (VAV3 and LYN) and a large array of NK receptors (KIR2DL3, KIR2DL4, KIR2DL1, KIR3DL1, KIR2DS5, etc.). In addition, we identified up to 161 genes that encode transcriptional regulators, some of unknown function in CD8+ T cells, that were differentially expressed in the course of differentiation. Overall, these results provide new insights into the regulatory networks involved in memory CD8+ T cell maintenance and T cell terminal differentiation.
Epigenetic Networks Regulate the Transcriptional Program in Memory and Terminally Differentiated CD8+ T Cells.
Specimen part
View SamplesEpigenetic mechanisms play a critical role during differentiation of T cells by contributing to the formation of stable and heritable transcriptional patterns. To further study the mechanisms of memory maintenance in CD8+ T cells, we performed genome-wide analysis of DNA methylation, histone marking (H3K9Ac and H3K9me3) and gene expression profiles in naive, effector memory (EM) and terminally differentiated memory (TEMRA) cells. Our results indicate that DNA demethylation and histone acetylation are coordinated to generate the transcriptional program associated with memory cells. Conversely, EM and TEMRA cells share a very similar epigenetic landscape. Nonetheless, the TEMRA transcriptional program predicts an innate immunity phenotype associated with genes never reported in these cells, including several mediators of NK cell activation (VAV3 and LYN) and a large array of NK receptors (KIR2DL3, KIR2DL4, KIR2DL1, KIR3DL1, KIR2DS5, etc.). In addition, we identified up to 161 genes that encode transcriptional regulators, some of unknown function in CD8+ T cells, that were differentially expressed in the course of differentiation. Overall, these results provide new insights into the regulatory networks involved in memory CD8+ T cell maintenance and T cell terminal differentiation.
Epigenetic Networks Regulate the Transcriptional Program in Memory and Terminally Differentiated CD8+ T Cells.
Specimen part, Treatment
View SamplesCotton fiber were used for the expression analysis at different developmental stages
Transcriptome dynamics during fibre development in contrasting genotypes of Gossypium hirsutum L.
No sample metadata fields
View SamplesMicroglia-like cells and neural cells were generated from several hES and hIPS lines. As subset was characterized by RNA seq and compared to expression profiles of published primary and induced samples. ABSTRACT: Microglia, the only lifelong resident immune cells of the central nervous system (CNS), are highly specialized macrophages which have been recognized to play a crucial role in neurodegenerative diseases such as Alzheimer's, Parkinson's and Adrenoleukodystrophy (ALD). However, in contrast to other cell types of the human CNS, bona fide microglia have not yet been derived from cultured human pluripotent stem cells. Here we establish a robust and efficient protocol for the rapid production of microglia-like cells from human embryonic stem (ES) and induced pluripotent stem (iPS) cells that uses defined serum-free culture conditions. These in vitro pluripotent stem cell-derived microglia-like cells (termed pMGLs) faithfully recapitulate the expected ontogeny and characteristics of their in vivo counterparts and resemble primary fetal human and mouse microglia. We generated these cells from multiple disease-specific cell lines, and find that pMGLs derived from MeCP2 mutant hES cells are smaller than their isogenic controls. We further describe a culture platform to study integration and live behavior of pMGLs in organotypic 3D-cultures. This modular differentiation system allows the study of microglia in highly defined conditions, as they mature in response to developmentally relevant cues, and provides a framework to study the long-term interaction of microglia residing in a tissue-like environment. Overall design: Individual donors/genetic backgrounds. Dataset inlcudes 4 differentiated neural progenitor biological replicates (NPC1-4), 2 primary fetal microglia samples as reference, 5 induced microglia samples grown in basal medium (pMGL1-5), 3 induced microglia samples grown in neural conditioned medium (pMGL1-3+NCM)
Efficient derivation of microglia-like cells from human pluripotent stem cells.
Subject
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