Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25023556.fastq.gz | Fastqsanger.gz | |||
| SRR25023557.fastq.gz | Fastqsanger.gz | |||
| SRR25023558.fastq.gz | Fastqsanger.gz | |||
| SRR25023559.fastq.gz | Fastqsanger.gz |
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Project description:Single-cell RNA-sequencing was performed on the tumor microenvironment of the glioblastomas isolated from PDOX models (Golebiewska et al., Acta Neuropathologica, 2020; Oudin et al., STAR Protocols 2021). Sample names correspond to PDOX models. Normal mouse brain was used as a contol. One PDOX model was treated with temolozomide (P3TMZ).
2023-03-07 | GSE226468 | GEO
Project description:Newcastle disease virus (NDV) has emerged as an oncolytic agent in several cancers. Previous study has shown that NDV exerts cytolytic activity in glioma, however, the underlying mechanism has not been fully uncovered. Here the cytolytic activity of NDV in glioma and the associated mechanisms have been demonstrated. Infection with NDV inhibits cell proliferation and promotes cell apoptosis in LN229 cells. Further investigation showed that cytoplasmic organelle damage and cytoplasmic vacuolation were observed in LN229 cells after NDV infection. JC-1 staining assay proved that NDV caused cell apoptosis of LN229 cells by inducing mitochondrial dysfunction. We next speculated that NDV caused LN229 cells death through inducing necroptosis, but not ferroptosis, since the Fe2+ level did not alter after NDV infection. Furthermore, the NDV-caused cell death in LN229 cells was blocked by necroptosis inhibitor Nec1. Besides, RNA-seq analysis identified the different expression genes in NDV-infected LN229 cells. OASL, an antiviral gene, has been found to be directly induced by NDV infection. We also found that knockdown of OASL enhanced NDV infection-induced LN229 cells necroptosis. In summary, two aspects about cytolytic activity of NDV in glioma have been demonstrated. NDV presented cytolytic activity in glioma cells through inducing necroptosis. Additionally, targeting OASL may provide new strategy for enhancing necroptosis of glioma cells after NDV infection.
2023-05-01 | GSE227791 | GEO
Project description:The NDV GM strain was used to infect DEF cells with 1moi, while an uninfected group was set up as a control. Changes in transcript levels of different genes after NDV infection of duck cells were identified by high-throughput sequencing. It is hoped to reveal the unique antiviral mechanism of waterfowl in resisting NDV infection.
2023-04-11 | GSE229234 | GEO
Project description:To investigate the role of gene expression during Newcastle disease virus (NDV) infection.The NDV GM strain was used to infect DEF cells with 1moi, while an uninfected group was set up as a control.
2023-04-11 | GSE229335 | GEO
Project description:Genotype VIId NDV is characterized by severe tissue damage in chicken lymphoid organs compared to other virulent strains. However, biological basis of this unusual pathological phenotype is unknown. Host response is associated with pathogenicity of Newcastle Disease Virus (NDV). We aim to determine the contribution of host response to the severe tissue destruction in the lymphoid system caused by genotype VIId NDV. We used microarray analysis to evaluate the global transcriptional response in the spleen of chickens infected with genotype VIId NDV strain JS5/05 and genotype IV NDV Herts/33.
2012-08-15 | GSE40100 | GEO
Project description:Nuclear localization of cytoplasmic RNA virus proteins mediated by intrinsic nuclear localization signal (NLS) plays essential roles in successful virus replication. We previously reported that NLS mutation in the matrix (M) protein obviously attenuates the replication and pathogenicity of Newcastle disease virus (NDV), but the attenuated replication mechanism of NDV remains unclear. In this study, we showed that M/NLS mutation not only disrupted M’s nucleocytoplasmic trafficking characteristic but also impaired viral RNA synthesis and transcription. Using TMT-based quantitative proteomics analysis of BSR-T7/5 cells infected with the parental NDV rSS1GFP and the mutant NDV rSS1GFP-M/NLSm harboring M/NLS mutation, we found that rSS1GFP infection stimulated much greater quantities and more expression level changes of differentially expressed proteins involved in host cell transcription, ribosomal structure, posttranslational modification, and intracellular trafficking than rSS1GFP-M/NLSm infection. Further in-depth analysis revealed that early nuclear localization of M protein inhibited cell transcription and participated in reducing cellular protein synthesis, posttranscriptional modification and transport; whereas later cytoplasmic localization of M protein promoted viral protein synthesis and benefited for virus assembly and budding. Importantly, we first demonstrated that later cytoplasmic localization of M protein effected the inhibition of TIFA expression in a dose-dependent manner, and inhibiting TIFA expression was beneficial to NDV replication by down-regulating TIFA/TRAF6/NF-κB-mediated production of cytokines. Our findings suggest that precocious cytoplasmic localization of M protein caused by M/NLS mutation disrupts these important biological processes, and thereby causes the attenuated replication of NDV, demonstrating that NDV replication is closely related to the nucleocytoplasmic trafficking of M protein.
2020-05-22 | PXD018098 | Pride