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Transcriptional effects of HSV-1-ICP0 and Ad5-E4ORF3 expression in BLaER1 monocytes [Virulence factors]

ABSTRACT: We have identified that the viral virulence factors ICP0 from HSV-1 and E4ORF3 from Adenovirus5 can activate the MORC3 pathway of innate immune sensing. To study the global transcriptional effects of virulence factor sensing, we overexpressed mCherry or these virulence factors from a doxycycline-inducible lentiviral construct in BLaER1 monocytes of various genotypes and performed RNA-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE182754 | GEO | 2021/11/01

REPOSITORIES: GEO

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Transcriptional effects of HSV-1-ICP0 and Ad5-E4ORF3 expression in BLaER1 monocytes [Virulence factors]

Project description:Transcriptional effects of HSV-1-ICP0 and Ad5-E4ORF3 expression in BLaER1 monocytes [Virulence factors]

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Transcriptional profile of MORC3 deficient BLaER1 monocytes [KO]

Project description:We have identified MORC3 as a negative regulator of Type I Interferon (IFN), whose absence induces IFN and interferon-stimulated genes (ISGs). To study the global transcriptional effects of loss of MORC3, we deleted MORC3 in WT, IFNAR1–/– IFNAR2–/– and IFNB1–/– BLaER1 monocytes and performed RNA-seq.

2021-11-01 | GSE182755 | GEO

ATAC-seq of MORC3 deficient BLaER1 monocytes [ATAC-seq]

Project description:We have identified MORC3 as a negative regulator of Type I Interferon (IFN), whose absence induces IFN and interferon-stimulated genes (ISGs). To study the global effects of MORC3 on DNA accessibility, we deleted MORC3 in IFNAR1-/- IFNAR2-/- BLaER1 monocytes and performed ATAC-seq.

2021-11-01 | GSE182752 | GEO

Transcriptional profile of MRE deficient BLaER1 monocytes [RNA MRE]

Project description:We have identified a MORC3-regulated DNA element (MRE) that regulates the activation of IFNB1 upon loss of MORC3. To study the global transcriptional effects of the MRE, we deleted the MRE in STAT1–/– STAT2–/– and STAT1–/– STAT2–/– MORC3–/– BLaER1 monocytes and performed RNA-seq.

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Transcriptional profile of MORC3 deficient BLaER1 monocytes [KO]

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ATAC-seq of MORC3 deficient BLaER1 monocytes [ATAC-seq]

Project description:ATAC-seq of MORC3 deficient BLaER1 monocytes [ATAC-seq]

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DNA-PK Phosphoproteomic Profiling during HSV-1 and DNA

Project description:HFF cells were infected with ICP0 RF HSV-1 (MOI 5), treated with bleomycin (10mg/mL), or left untreated as a control. Nu-7441 (DNA-PK inhibitor; 2uM)or DMSO (Control) was applied after 1 hour then samples were harvested after 1 hour for bleomycin treated cells or 6 hours for HSV-1 infected cells.

2024-10-07 | PXD044489 | Pride

Identification of viral and host targets of miR-138 by PAR-CLIP analysis of herpes simplex virus 2 infected 293T cells

Project description:Like herpes simplex virus 1 (HSV-1) ICP0 mRNA, HSV-2 ICP0 mRNA is predicted to be targeted by a host neuron-specific microRNA, miR-138. This study was designed to confirm the interaction between HSV-2 ICP0 mRNA and miR-138, and to identify other potential viral and host targets of miR-138 during HSV-2 infection. We performed PAR-CLIP on HSV-2 infected 293T cells overexpressing miR-138 in comparisin to control 293T cells. The results confirmed ICP0 as miR-138's targets, and also identified some other potential viral and host targets of miR-138.

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TAP/MS of enriched ICP0 gel detection in human astroblastoma cells infected with HSV-1

Project description:TAP/MS of enriched ICP0 gel detection in human astroblastoma cells infected with HSV-1 to identify ICP0's interacting partners

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Identification of targets of miR-138 in Neuro-2a and 293T cells by RNAseq

Project description:We previously showed that miR-138 can repress herpes simplex virus 1 (HSV-1) ICP0 expression by binding to ICP0 mRNA. However, in this study we found that miR-138 can also repress viral gene expression independent of ICP0. We did not find other confirmed viral targets of miR-138. Therefore we conducted these RNAseq experiments (in combination with PAR-CLIP experiments whose results are uploaded separately) to identify host targets of miR-138 in two cell lines to explain the ICP0-independent effects on HSV-1 gene expression.

2020-04-27 | GSE127502 | GEO

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