Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA265057 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Differential gene expression in human THP-1 monocytes expressing the RdRP transgene (WT version) compared to THP-1 empty vector control cells
| PRJNA265058 | ENA
Project description:Differential gene expression in human THP-1 monocytes expressing the RdRP∆rna mutant transgene compared to THP-1 empty vector control cells
| PRJNA265056 | ENA
Project description:Previously, we reported that mice made transgenic for a picornaviral RdRP â?? the 3Dpol protein of Theilerâ??s murine encephalomyelitis virus (TMEV) â?? suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNαβR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRPâ??rna). Another mutant, RdRPâ??cat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRPâ??rna, and RdRPâ??cat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated. RdRP cDNAs and a GFP-puromycin fusion protein selection marker were cloned into transfer constructs containing HIV LTRs, a small portion of gag, an RRE, and a cPPT. Transfer constructs were transfected into HEK 293T cells along with packaging construct Râ??8.9 and envelope pseudotyping construct expressing VSV-G. RT-normalized amounts of vector were used to transduce THP-1 cells. After selection in puromycin, whole-genome expression profiling was performed on total RNA extracted from the different THP-1 lines.
2015-11-08 | E-GEOD-62754 | biostudies-arrayexpress
Project description:Previously, we reported that mice made transgenic for a picornaviral RdRP â the 3Dpol protein of Theilerâs murine encephalomyelitis virus (TMEV) â suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNαβR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRPârna). Another mutant, RdRPâcat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRPârna, and RdRPâcat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated. RdRP cDNAs and a GFP-puromycin fusion protein selection marker were cloned into transfer constructs containing HIV LTRs, a small portion of gag, an RRE, and a cPPT. Transfer constructs were transfected into HEK 293T cells along with packaging construct Râ8.9 and envelope pseudotyping construct expressing VSV-G. RT-normalized amounts of vector were used to transduce THP-1 cells. After selection in puromycin, whole-genome expression profiling was performed on total RNA extracted from the different THP-1 lines.
2015-11-08 | E-GEOD-62753 | biostudies-arrayexpress
Project description:Previously, we reported that mice made transgenic for a picornaviral RdRP â the 3Dpol protein of Theilerâs murine encephalomyelitis virus (TMEV) â suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNαβR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRPârna). Another mutant, RdRPâcat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRPârna, and RdRPâcat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated. RdRP cDNAs and a GFP-puromycin fusion protein selection marker were cloned into transfer constructs containing HIV LTRs, a small portion of gag, an RRE, and a cPPT. Transfer constructs were transfected into HEK 293T cells along with packaging construct Râ8.9 and envelope pseudotyping construct expressing VSV-G. RT-normalized amounts of vector were used to transduce THP-1 cells. After selection in puromycin, whole-genome expression profiling was performed on total RNA extracted from the different THP-1 lines.
2015-11-08 | E-GEOD-62755 | biostudies-arrayexpress
Project description:Previously, we reported that mice made transgenic for a picornaviral RdRP – the 3Dpol protein of Theiler’s murine encephalomyelitis virus (TMEV) – suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNαβR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRP∆rna). Another mutant, RdRP∆cat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRP∆rna, and RdRP∆cat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated.
2015-11-08 | GSE62755 | GEO
Project description:Previously, we reported that mice made transgenic for a picornaviral RdRP – the 3Dpol protein of Theiler’s murine encephalomyelitis virus (TMEV) – suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNαβR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRP∆rna). Another mutant, RdRP∆cat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRP∆rna, and RdRP∆cat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated.
2015-11-08 | GSE62754 | GEO
Project description:Previously, we reported that mice made transgenic for a picornaviral RdRP – the 3Dpol protein of Theiler’s murine encephalomyelitis virus (TMEV) – suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNαβR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRP∆rna). Another mutant, RdRP∆cat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRP∆rna, and RdRP∆cat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated.
2015-11-08 | GSE62753 | GEO
Project description:We investigated whether UTX condensates regulate local H3K4me1 in the genome by ChIP-seq of THP-1 cells expressing empty vector (control), UTX WT, ΔcIDR, UTX-eIFIDR, or ΔTPR. To determine the effect of UTX condensation on high-order chromatin interactions or looping, we performed H3K4me3 HiChIP in duplicates to generate high-resolution contact maps around the active and poised transcription start sites (TSSs) in THP-1 cells expressing empty vector (control), UTX WT, ΔcIDR, or UTX-eIFIDR.
2021-07-15 | GSE149420 | GEO
Project description:The hairy cell leukemia line JOK1 with low RhoH expression was stably trasfected with either an empty expression vector or this same vector expressing human RhoH. The transcriptomes of these two daughter lines were then compared by differential microarray analysis The hairy cell leukemia line JOK1 with low RhoH expression was stably trasfected with either an empty expression vector or this same vector expressing human RhoH. The transcriptomes of these two daughter lines were then compared by differential microarray analysis
2021-01-03 | GSE156483 | GEO