Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA244012 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from human monocyte derived dendritic cells infected with adenovirus expressing HIV-1 Vpr
| PRJNA260396 | ENA
Project description:HIV-1 Vpr protein is a multifunctional protein which perturbs human transcriptome and interacts with a number of cellular proteins. In this study, we have attempted to explore the efffects of Vpr on human transcriptome and have identified several genes which are involved in innate immune respone and cell signaling pathways. We used the microarray analysis to elucidate the differnetail expression pattern of differnet genes in human macrophages infected with HIV-1 Vpr. As result we found that HIV-1 Vpr protein leads to the induction of various interferon stimualted genes (ISGs) and chemokines in human macrophages. Human monocytes-derived macrophages (MDMs) were isolated from peripheral blood mononuclear cells (PBMCs) from two healthy donors and were infected with recombinant adenoviruses either expressing HIV-1 Vpr or ZsGreen1 as a control. At 48 hours post-infection, RNA was isolated and subjected to microarray analysis.
2014-04-09 | E-GEOD-56591 | biostudies-arrayexpress
Project description:HIV-1 Vpr protein is a multifunctional protein which perturbs human transcriptome and interacts with a number of cellular proteins. In this study, we have attempted to explore the efffects of Vpr on human transcriptome and have identified several genes which are involved in innate immune responses. We used the microarray analysis to elucidate the differnetail expression pattern of differnet genes in human dendritic cells infected with HIV-1 Vpr. As result we found that HIV-1 Vpr protein leads to the induction of various interferon stimualted genes (ISGs) in human monocyte derived dendritic cells. Human monocytes-derived dendritic cells (MDDCs) were isolated from peripheral blood mononuclear cells (PBMCs) from two healthy donors and were infected with recombinant adenoviruses either expressing HIV-1 Vpr or ZsGreen1 as a control. At 48 hours post-infection, RNA was isolated and subjected to microarray analysis.
2014-09-06 | E-GEOD-61171 | biostudies-arrayexpress
Project description:HIV-1 Vpr protein is a multifunctional protein which perturbs human transcriptome and interacts with a number of cellular proteins. In this study, we have attempted to explore the efffects of Vpr on human transcriptome and have identified several genes which are involved in innate immune responses. We used the microarray analysis to elucidate the differnetail expression pattern of differnet genes in human dendritic cells infected with HIV-1 Vpr. As result we found that HIV-1 Vpr protein leads to the induction of various interferon stimualted genes (ISGs) in human monocyte derived dendritic cells.
2014-09-06 | GSE61171 | GEO
Project description:HIV-1 Vpr protein is a multifunctional protein which perturbs human transcriptome and interacts with a number of cellular proteins. In this study, we have attempted to explore the efffects of Vpr on human transcriptome and have identified several genes which are involved in innate immune respone and cell signaling pathways. We used the microarray analysis to elucidate the differnetail expression pattern of differnet genes in human macrophages infected with HIV-1 Vpr. As result we found that HIV-1 Vpr protein leads to the induction of various interferon stimualted genes (ISGs) and chemokines in human macrophages.
2014-04-09 | GSE56591 | GEO
Project description:HIV-1 infection of monocyte-derived macrophages does not elicit a detectable type I IFN response in vitro, however, previously published data has shown that blocking STAT1 and STAT3 inhibits HIV-1 replication. Here we test to see if low levels of IFN inducible genes are detectable in human monocyte-derived macrophages that have been infected with HIV-1 in vitro.
2018-01-09 | GSE108897 | GEO
Project description:Lentiviral accessory genes enhance replication through diverse mechanisms. HIV-1 accessory protein Vpr modulates the host DNA damage response (DDR) at multiple steps through DNA damage, cell cycle arrest, the degradation of host proteins, and both the activation and repression of DDR signaling. Vpr also alters host and viral transcription; however, the connection between Vpr-mediated DDR modulation and transcriptional activation remains unclear. Here, we determined the cellular consequences of Vpr-induced DNA damage using Vpr mutants that allow us to separate the ability of Vpr to induce DNA damage from cell cycle arrest and other DDR phenotypes including host protein degradation and repression of DDR. RNA-sequencing of cells expressing Vpr or Vpr mutants identified that Vpr alters cellular transcription through mechanisms both dependent and independent of cell cycle arrest. In tissue-cultured U2OS cells and primary human monocyte-derived macrophages (MDMs), Vpr-induced DNA damage activates the ATM-NEMO pathway and alters cellular transcription via NF-κB/RelA signaling. HIV-1 infection of primary MDMs validated Vpr-dependent NF-κB transcriptional activation during infection. Both virion delivered and de novo expressed Vpr induced DNA damage and activated ATM-NEMO dependent NF-κB transcription, suggesting that engagement of the DDR and transcriptional reprogramming can occur during early and late stages of viral replication. Together, our data identifies a mechanism by which Vpr activates NF-κB through DNA damage and the ATM-NEMO pathway, which occur independent of cell cycle arrest. We propose this is essential to overcoming restrictive environments, such as in macrophages, to enhance viral transcription and replication.
2024-08-23 | GSE253779 | GEO
Project description:HIV-1 accessory protein, Vpr, is required for efficient HIV-1 infection of macrophages. Here we show that Vpr reprograms macrophage gene expression by altering the activity of master transcriptional regulator, PU.1, which is responsible for regulating the expression of host immune response genes and is necessary for normal hematopoiesis. In HIV-infected primary macrophages, Vpr-dependent changes in PU.1 levels result in suppression of known anti-viral targets of Vpr including IFITM3 and MRC1. Moreover, we find that PU.1 and its co-factor TET2 are co-recruited to DCAF1 by Vpr and targeted for accelerated degradation. Downmodulation of PU.1 is a highly conserved function of Vpr that is maintained across primate lentiviruses including HIV-2 and several SIVs. In contrast, this activity is not shared by the evolutionarily related accessory protein Vpx. Our findings demonstrate how Vpr dramatically enhances HIV spread in macrophages by targeting a myeloid-specific transcription factor needed for expression of multiple viral restriction factors.
2024-04-30 | GSE220574 | GEO
Project description:Transcriptional profiling of HIV-1 infected and that of IFNbeta, IFNgamma or LPS stimulated human monocyte derived macrophages.
2009-09-01 | E-MEXP-2032 | biostudies-arrayexpress
Project description:Whole genome expression profiling of HIV-1 infected and uninfected monocyte-derived macrophages
2009-01-01 | E-MEXP-1904 | biostudies-arrayexpress