Ontology highlight
ABSTRACT:
PROVIDER: PRJNA623580 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11499055_1.fastq.gz | Fastqsanger.gz | |||
| SRR11499056_1.fastq.gz | Fastqsanger.gz | |||
| SRR11499057_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
Project description:Murine gammaherpesvirus 68 (MHV-68) is closely related to Epstein-Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) and provides a small animal model to study the pathogenesis of gammaherpesvirus (γHV) infections. To completely explore the potential of the MHV-68 system for the investigation of gHV miRNAs, it would be desirable to know the number and expression patterns of all miRNAs encoded by MHV-68. By using small RNA deep sequencing, we systematically investigated the MHV-68 miRNA expression profiles in both lytically and persistently infected cells. In addition to the known nine MHV-68 miRNAs, we identified six novel MHV-68 miRNA genes and analyzed the expression levels of all MHV-68 miRNAs. Furthermore, we also characterized the cellular miRNA expression signatures in MHV-68 infected versus non-infected NIH3T3 fibroblasts and in TPA-treated versus non-treated S11 cells. We found that mmu-mir-15b and mmu-mir-16 are highly upregulated upon MHV-68 infection of NIH3T3 cells, indicating a potential role of cellular miRNAs during MHV-68 infection. Our data will aid to fully explore the functions of gHV miRNAs.
2010-07-15 | GSE22938 | GEO
Project description:Murine gammaherpesvirus 68 (MHV-68) is closely related to Epstein-Barr virus (EBV) and KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV) and provides a small animal model to study the pathogenesis of gammaherpesvirus (M-NM-3HV) infections. To completely explore the potential of the MHV-68 system for the investigation of gHV miRNAs, it would be desirable to know the number and expression patterns of all miRNAs encoded by MHV-68. By using small RNA deep sequencing, we systematically investigated the MHV-68 miRNA expression profiles in both lytically and persistently infected cells. In addition to the known nine MHV-68 miRNAs, we identified six novel MHV-68 miRNA genes and analyzed the expression levels of all MHV-68 miRNAs. Furthermore, we also characterized the cellular miRNA expression signatures in MHV-68 infected versus non-infected NIH3T3 fibroblasts and in TPA-treated versus non-treated S11 cells. We found that mmu-mir-15b and mmu-mir-16 are highly upregulated upon MHV-68 infection of NIH3T3 cells, indicating a potential role of cellular miRNAs during MHV-68 infection. Our data will aid to fully explore the functions of gHV miRNAs. A mouse fibroblast cell line infected with/without MHV-68 and a MHV-68 infected mouse B lymphoma cell line treated with/without TPA (4 samples in total) were examined.
2010-07-15 | E-GEOD-22938 | biostudies-arrayexpress
Project description:To investigate the transcriptome differences between wild-type and ZUP1 knock-out mice in liver when they were infected with MHV, we employed MHV-A59, a hepatic and neuronal tropic murine coronavirus, to infect wild-type and Zup1 knockout mice and colleted liver tissues after MHV infection to perform RNA- sequencing.
2025-01-16 | GSE286528 | GEO
Project description:RNA-sequencing data of mock, wild-type, and EndoUmut MHV A59 infected IFNAR-/- bone-marrow derived macrophages. RNA was isolated at 6 hours post infection and immunoprecipitated with anti-dsRNA antibody to determine which RNA are forming a dsRNA epitope during viral infection. RNAs were mapped to C57Bl/6 Mouse genome or MHV-A59 genome (Genbank accession # AY910861).
2020-02-07 | GSE144886 | GEO
Project description:Pre- and post-transcriptional mechanisms, including alternative promoters, termination signals, and splicing, play essential roles in diversifying protein output by generating distinct RNA and protein isoforms. Two major challenges in characterizing the cellular function of alternative isoforms are the lack of experimental methods to specifically and efficiently modulate isoform expression and computational tools for complex experimental design and analysis. To address these gaps, we developed and methodically tested an isoform-specific knockdown strategy which pairs the RNA-targeting CRISPR/Cas13d system with guide RNAs that span exon-exon junctions in the mature RNA. We performed a high-throughput essentiality screen, quantitative RT-PCR assays, and PacBio long read sequencing to affirm our ability to specifically target and robustly knockdown individual RNA isoforms. Using the example gene RBFOX2, we validated protein-level changes and assessed the functional impact of isoform-specific knockdown. In parallel, we provide computational tools for experimental design and screen analysis. Considering all possible splice junctions annotated in GENCODE for multi-isoform genes and our gRNA efficacy predictions, we estimate that our junction-centric strategy can uniquely target up to 89% of human RNA isoforms, including 50,066 protein-coding and 11,415 lncRNA isoforms. Importantly, this specificity spans all transcriptional and splicing events, including exon skipping and inclusion, alternative 5’ and 3’ splice sites, and alternative starts and ends.
2025-06-25 | PXD060902 | panorama
Project description:The mouse hepatitis virus (MHV) genomic and sub-genomic RNAs have 3’ poly(A) tails. The terminal addition of uridines to poly(A) tails has been shown to be a widespread modification. Here, we investigated the presence of 3' end additions on the MHV RNA poly(A) tails. To this end, we infected NCTC cells with MHV and isolated RNA at 24-hours post-infection (hpi). While the median poly(A) tail length of the MHV RNAs is around 50 nucleotides, we observed a peak of uridylation in transcripts with poly(A) tails about 40 nucleotides long
2023-03-23 | GSE200414 | GEO