MiRNA expression profiles in YT and NK92 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Chung-Wu Lin
PROVIDER: E-GEOD-53476 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The miRNA expression profiles of of EBV-infected YT and NK92 cells are compared. YT cells have weaker expression of T-bet and IFNg than NK92 cells. It was found that the EBV-encoded miR-BART20-5p inhibits the expression of T-bet and IFNg in YT cells.
2014-01-21 | GSE53476 | GEO
Project description:YT and NK92 cells are EBV-infected lymphoma cells of NK- cell origin. YT cells have weaker expression of T-bet and IFNg than NK92 cells. However, this data set shows that both cell lines have similar mRNA levels, implying post-transcriptional regulations. Affymetrix chips (Human Genome U133 plus 2.0) were used for a genome-wide screen of transcriptional profiles on YT and NK cells. Hybridization and washing of the arrays were done according to the GeneChip® Expression Analysis Technical Manual from Affymetrix. The arrays were scanned with GenePix 4000B (Molecular Devices, Sunnyvale, CA.), and the data were extracted with Affymetrix Microarray suite (MAS) software.
2014-01-21 | E-GEOD-53478 | biostudies-arrayexpress
Project description:YT and NK92 cells are EBV-infected lymphoma cells of NK- cell origin. YT cells have weaker expression of T-bet and IFNg than NK92 cells. However, this data set shows that both cell lines have similar mRNA levels, implying post-transcriptional regulations.
2014-01-21 | GSE53478 | GEO
Project description:T-bet is a critical transcription factor for T helper 1 (Th1) cell differentiation. To study the regulation and functions of T-bet, we developed a T-bet-ZsGreen reporter mouse strain, in which GFP faithfully reflects the expression of T-bet. By using this tool, we report that signals elicited by IL-12 and IFNg are redundant in inducing T-bet in mice infected with Toxoplasma gondii and that T-bet does not contribute to its own expression when induced by IL-12 and IFNg. While both T-bet and Stat4 are critical for IFNg production, IFNg signaling is dispensable. Strikingly, loss of T-bet results in activation of an endogenous Th2 program in cells expressing T-bet-ZsGreen. Genome-wide analyses suggest T-bet directly induces Th1-related genes but indirectly suppresses Th2-related genes. Our study revealed redundancy and synergy among several Th1-inducing pathways in regulating the expression of T-bet and IFNg, and a critical role of T-bet in suppressing an endogenous Th2 program. RNA-Seq experiments were performed using total RNAs isolated from both wild type and Tbx21-/- Th1 cells in duplicates. Tbet ChIP-seq was performed using wild type Th1 cells. H3K4me1 and H3K27me3 ChIP-seq was performed using both wild type and Tbx21-/- Th1 cells.
2012-10-04 | E-GEOD-38808 | biostudies-arrayexpress
Project description:In the current study, we examined the cellular and viral miRNA expression profile in KSHV-infected patients without clinical signs of KSHV-associated disease. In addition, we characterized the viral miRNAs encoded by KSHV and EBV during natural infections in these patients. Finally, we show that malaria infection results in major alterations of the molecular content of plasma exosomes.
2018-02-16 | PXD008107 | Pride
Project description:T-bet is a critical transcription factor for T helper 1 (Th1) cell differentiation. To study the regulation and functions of T-bet, we developed a T-bet-ZsGreen reporter mouse strain, in which GFP faithfully reflects the expression of T-bet. By using this tool, we report that signals elicited by IL-12 and IFNg are redundant in inducing T-bet in mice infected with Toxoplasma gondii and that T-bet does not contribute to its own expression when induced by IL-12 and IFNg. While both T-bet and Stat4 are critical for IFNg production, IFNg signaling is dispensable. Strikingly, loss of T-bet results in activation of an endogenous Th2 program in cells expressing T-bet-ZsGreen. Genome-wide analyses suggest T-bet directly induces Th1-related genes but indirectly suppresses Th2-related genes. Our study revealed redundancy and synergy among several Th1-inducing pathways in regulating the expression of T-bet and IFNg, and a critical role of T-bet in suppressing an endogenous Th2 program.
2012-10-04 | GSE38808 | GEO
Project description:Epstein-Barr virus (EBV) is a human herpesvirus linked to a number of B cell cancers and lymphoproliferative disorders. During latent infection, EBV expresses 25 viral pre-microRNAs (miRNAs) and induces the expression of specific host miRNAs, such as miR-155 and miR-21, which potentially play a role in viral oncogenesis. To date, a limited number of EBV miRNA targets have been identified; thus, the role of EBV miRNAs in viral pathogenesis is not well defined. Here, we used photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP) combined with deep sequencing and computational analysis to comprehensively examine the viral and cellular miRNA targetome in EBV B95-8-infected lymphoblastoid cell lines (LCLs). We identified 7,827 miRNA-interaction sites in 3,492 cellular 3'UTRs. 531 of these sites contained seed-matches to viral miRNAs. 24 PAR-CLIP-identified miRNA:3'UTR interactions were confirmed by reporter assays. Our results reveal that EBV miRNAs predominantly target cellular transcripts during latent infection, thereby manipulating the host environment. Furthermore, targets of EBV miRNAs are involved in multiple cellular processes that are directly relevant to viral infection, including innate immunity, cell survival, and cell proliferation. Finally, we present evidence that myc-regulated host miRNAs from the miR-17/92 cluster can regulate latent viral gene expression. This comprehensive survey of the miRNA targetome in EBV-infected B cells represents a key step towards defining the functions of EBV-encoded miRNAs, and potentially, identifying novel therapeutic targets for EBVassociated malignancies.
2012-10-16 | GSE41437 | GEO
Project description:Epstein-Barr virus (EBV) is a human herpesvirus linked to a number of B cell cancers and lymphoproliferative disorders. During latent infection, EBV expresses 25 viral pre-microRNAs (miRNAs) and induces the expression of specific host miRNAs, such as miR-155 and miR-21, which potentially play a role in viral oncogenesis. To date, a limited number of EBV miRNA targets have been identified; thus, the role of EBV miRNAs in viral pathogenesis is not well defined. Here, we used photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP) combined with deep sequencing and computational analysis to comprehensively examine the viral and cellular miRNA targetome in EBV B95-8-infected lymphoblastoid cell lines (LCLs). We identified 7,827 miRNA-interaction sites in 3,492 cellular 3'UTRs. 531 of these sites contained seed-matches to viral miRNAs. 24 PAR-CLIP-identified miRNA:3'UTR interactions were confirmed by reporter assays. Our results reveal that EBV miRNAs predominantly target cellular transcripts during latent infection, thereby manipulating the host environment. Furthermore, targets of EBV miRNAs are involved in multiple cellular processes that are directly relevant to viral infection, including innate immunity, cell survival, and cell proliferation. Finally, we present evidence that myc-regulated host miRNAs from the miR-17/92 cluster can regulate latent viral gene expression. This comprehensive survey of the miRNA targetome in EBV-infected B cells represents a key step towards defining the functions of EBV-encoded miRNAs, and potentially, identifying novel therapeutic targets for EBVassociated malignancies. Ago2 (Argonaute 2) PAR-CLIP and small RNA deep sequencing of Epstein-Barr virus B95.8-infected lymphoblastoid cell lines (LCLs).
2012-10-16 | E-GEOD-41437 | biostudies-arrayexpress
Project description:Nasopharyngeal carcinoma (NPC) is endemic in Southeast Asia and southern China. The primary treatment for NPC is radiotherapy. Despite of the encouraging results of radiotherapy, local recurrence or distant metastases of NPC after the initial therapy is frequently found due to radioresistance. Therefore, there is an urgent need to identify genes that control radiosensitivty, aiming to reduce disease recurrence. Epstein-Barr virus (EBV) infection was closely associated with undifferentiated NPC. EBV-encoded microRNAs (miRNAs) played crucial roles in the pathogenesis of NPC. Ebv-miR-BART7 belongs to the 44 EBV BART miRNAs and was found to be up-regulated in NPC tissues and plasma. Forced expression of ebv-miR-BART7 enhanced the radiosensitivity of NPC cells. However, the mechanisms underlying the sensitizing effect of ebv-miR-BART7 on radiation remain largely unknown. Given that miRNA exerts biological functions by regulating its targets, we used microarray to identify the targets of ebv-miR-BART7 that regulate radiosensitivity of NPC cells.
2017-03-31 | GSE79571 | GEO
Project description:The prototypic gammaherpesvirus Epstein-Barr virus (EBV) is carried by over 90% of the adult human population. Although infection often proceeds asymptomatically, the virus is causally involved in infectious mononucleosis and various malignancies. Like all herpesviruses, EBV establishes a lifelong latent infection in its human host. To successfully establish a persistent infection and spread to new hosts, EBV needs to avoid clearance by the host immune system. In addition to ~100 proteins, some of which perform immunomodulatory functions, EBV encodes over 40 mature miRNAs. Cellular miRNAs regulate diverse cellular processes, but the functions of the EBV miRNAs remain poorly understood. In this study, we identify EBV-encoded miR-BART16 as a novel viral immune evasion factor that interferes with host type I IFN responses. miR-BART16-5p downregulates the cellular histone acetyltransferase CBP (CREBB-binding protein) by directly targeting the CBP-encoding mRNA. CBP plays an important role in the type I IFN signaling pathway. Inhibiting endogenously expressed miR-BART16 in EBV-transformed B cells and gastric carcinoma cells results in increased CBP levels. Consistent with the important role of CBP in type I IFN signaling, miR-BART16 expression interferes with ISRE-promoter activity and production of interferon-stimulated genes in response to IFN-α treatment. These combined data show that EBV employs miRNAs to modify IFN-induced gene transcription. Given the importance of the host IFN system in the antiviral defence, obstructing this response may provide a way for EBV to favour viral replication and could play an etiological role in EBV-associated malignancies.
2017-04-05 | GSE69697 | GEO