Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MRNA sequencing of human glioma stem like cell and Kaposi's sarcoma assocaited herpesvirs infected human glioma stem like cell.

ABSTRACT: Difference of cell growth between KSHV infected human glioblastoma stem like cell and uninfected cell.

ORGANISM(S): Homo sapiens

PROVIDER: GSE100013 | GEO | 2020/06/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Unveiling the Role of KSHV-Infected Human Mesenchymal Stem Cells in Kaposi's Sarcoma Initiation

Project description:Kaposi's sarcoma (KS) may derive from Kaposi's Sarcoma Herpesvirus (KSHV)-infected human Mesenchymal Stem Cells (hMSCs) that migrate to sites characterized by inflammation and angiogenesis, promoting the initiation of KS. By analyzing the RNA sequences of KSHV-infected primary hMSCs, we have identified specific cell subpopulations, mechanisms, and conditions involved in the initial stages of KSHV-induced transformation and reprogramming of hMSCs into KS progenitor cells. Under pro-angiogenic environmental conditions, KSHV can reprogram hMSCs to exhibit gene expression profiles more similar to KS tumors, activating cell cycle progression, cytokine signaling pathways, and endothelial differentiation indicating the involvement of KSHV infection in inducing the Mesenchymal-to-Endothelial (MEndT) transition of hMSCs. This finding underscores the significance of this condition in facilitating KSHV-induced proliferation and reprogramming of hMSCs towards MEndT and closer to KS gene expression profiles, providing further evidence of these cell subpopulations as precursors of KS cells that thrive in a pro-angiogenic environment.

2024-07-08 | GSE260925 | GEO

Deregulation of lncRNAs by Kaposi's sarcoma-associated herpesvirus

Project description:Deregulation of host lncRNAs following infection with Kaposi’s sarcoma-associated herpesvirus (KSHV) was assessed. Total RNA was prepared from uninfected TIVE cells (telomerase-immortalized vein endothelial cells), and from TIVE cells latently infected with either wild-type KSHV or with a deletion mutant (Δcluster-KSHV) lacking ten of the twelve KSHV microRNA genes. The RNA was converted to labeled cRNA and used to probe a human lncRNA microarray. The goal was to investigate which host lncRNAs were either up- or down-regulated during latent infection with KSHV, and to determine if deregulation of host lncRNAs was dependent on KSHV miRNAs.

2017-07-12 | GSE89114 | GEO

Expression data of extracellular vesicles from kaposi's sarcoma associated herpesvirus- or mock- infected human endothelial cells treated human endothelial cell

Project description:Kaposi’s Sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi’s sarcoma, which is the most common cancer in acquired immune deficiency syndrome patients. Because KSHV has many viral proteins modulate many response, However, various effects by extracellular vesicles (EVs) during de novo KSHV infection has not been investigated to our best knowledge. We used microarrays to detail of gene expression underlying EV treatment and identified the up-regulated genes during treatment.

2018-10-16 | GSE121220 | GEO

Differentially regulated splice variants and systems biology analysis of Kaposi's Sarcoma-associated Herpesvirus-infected lymphatic endothelial cells

Project description:Alternative RNA splicing greatly increases proteome diversity, and the possibility of studying genome-wide alternative splicing (AS) events becomes available with the advent of high-throughput genomics tools devoted to this issue. Kaposi’s sarcoma associated herpesvirus (KSHV) is the etiological agent of KS, a tumor of lymphatic endothelial cell (LEC) lineage, but little is known about the AS variations induced by KSHV. We analyzed KSHV-controlled AS using high-density microarrays capable of detecting all exons in the human genome. Splicing variants and altered exon-intron usage in infected LEC were found, and these correlated with protein domain modification. The different 3’ UTR used in new transcripts also help isoforms to escape microRNA-mediated surveillance. Exome-level analysis further revealed information that cannot be disclosed using classical gene-level profiling: a significant exon usage difference existed between LEC and CD34+ precursor cells, and KSHV infection resulted in LEC-to-precursor, dedifferentiation-like exon level reprogramming. Our results demonstrate the application of exon arrays in systems biology research, and suggest the regulatory effects of AS in endothelial cells are far more complex than previously observed. This extra layer of molecular diversity helps to account for various aspects of endothelial biology, KSHV life cycle and disease pathogenesis that until now have been unexplored. 5 samples were analyzed. 3 were KSHV infected lymphatic endothelial cells (LECs), and 2 were non-infected control samples.

2011-05-05 | E-GEOD-26341 | biostudies-arrayexpress

mECK36: a cell and animal model of virally induced Kaposi's sarcoma

Project description:Transfection of a Kaposi's sarcoma (KS) herpesvirus (KSHV) Bacterial Artificial Chromosome (KSHVBac36) into mouse bone marrow endothelial lineage cells generated a cell (mECK36) that induced KS-like tumors in mice. mECK36 formed KSHV-harboring vascularized spindle-cell sarcomas that were LANA+ and displayed a KSHV and host transcriptomes reminiscent of KS tumors. Keywords: Cell type comparison

2007-01-01 | GSE6482 | GEO

Unveiling the role of KSHV-infected human mesenchymal stem cells in Kaposi's sarcoma initiation.

Project description: Not available

| S-EPMC12068558 | biostudies-literature

The Open Chromatin Landscape of Kaposi's Sarcoma-Associated Herpesvirus

Project description:KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus which establishes latent infection in endothelial and B cells, as well as in primary effusion lymphoma (PEL). During latency, the viral genome exists as a circular DNA minichromosome (episome) and is packaged into chromatin analogous to human chromosomes. Only a small subset of promoters, those which drive latent RNAs, are active in latent episomes. In general, nucleosome depletion (M-bM-^@M-^\open chromatinM-bM-^@M-^]) is a hallmark of eukaryotic regulatory elements such as promoters and transcriptional enhancers or insulators. We applied formaldehyde-assisted isolation of regulatory elements (FAIRE) followed by next-generation sequencing to identify regulatory elements in the KSHV genome and integrated these data with previously identified locations of histone modifications, RNA polymerase II occupancy, and CTCF binding sites. We found that (i) regions of open chromatin were not restricted to the transcriptionally defined latent loci; (ii) open chromatin was adjacent to regions harboring activating histone modifications, even at transcriptionally inactive loci; and (iii) CTCF binding sites fell within regions of open chromatin with few exceptions, including the constitutive LANA promoter and the vIL6 promoter. FAIRE-identified nucleosome depletion was similar among B and endothelial cell lineages, suggesting a common viral genome architecture in all forms of latency. Ten total samples analyzed by FAIRE-seq from latent KSHV-infected cell lines. Two replicates were performed for BC1, KSHV-BJAB, KSHV-HUVEC, and L1-TIVE cells using the Illumina HiSeq 2000 platform. For BCBL1 cells, 1 FAIRE-seq sample and 1 non-cross-linked control BCBL1 sample was analyzed using the Illumina GAIIx

2013-09-05 | E-GEOD-50581 | biostudies-arrayexpress

Differentially regulated splice variants and systems biology analysis of Kaposi's Sarcoma-associated Herpesvirus-infected lymphatic endothelial cells

2011-05-05 | GSE26341 | GEO

KSHV-infected invasive bladder cancer cell: Control vs. KSHV-infected

Project description:Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells. Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells.

2015-03-10 | E-GEOD-66682 | biostudies-arrayexpress

KSHV-infected invasive bladder cancer cell: Control vs. KSHV-infected

Project description:Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells.

2015-03-10 | GSE66682 | GEO