Ontology highlight
ABSTRACT:
PROVIDER: PRJNA554675 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Integrase CLIP-seq experiments were conducted on wild-type and eccentric HIV-1 virions generated in the presence of allosteric integrase inhibitors and IN K264/266A and R269/K273A mutations Integrase CLIP-seq experiments were conducted by immunoprecipitation of integrase-RNA complexes from fully formed mature and eccentric virus particles. Libraries of RNA molecules bound by integrase were generated and sequenced by Illumina Hi-Seq2000 and 2500 platforms.
2016-08-25 | E-GEOD-83588 | biostudies-arrayexpress
Project description:Integrase CLIP-seq experiments were conducted on wild-type and eccentric HIV-1 virions generated in the presence of allosteric integrase inhibitors and IN K264/266A and R269/K273A mutations
2016-08-25 | GSE83588 | GEO
Project description:Identification of minority resistance mutations in the HIV-1 integrase gene using Next Generation Sequencing
| PRJEB9552 | ENA
Project description:HIV-1 infection of human monocyte-derived dendritic cells with and without the integrase inhibitor, Raltegravir
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Project description:Co-IP of HIV-1 integrase proteins - WT, K258R and K258/264/266/273R. Integrase proteins were cloned into a mammalian expression vector (pJET). All proteins had an N-terminal HA-tag used for IP. As a negative control, cells were transfected with an empty HA vector. Co-IPs were done in HEK293T cells.
2022-05-20 | PXD031825 | Pride
Project description:Distinct integration patterns of different retroviruses have puzzled virologists for over 20 years. The viral integrase (IN), as part of the intasome complex, docks onto the target DNA (tDNA) and catalyzes the insertion of the viral genome into the host chromatin. We identified retroviral IN amino acids directly contacting tDNA bases and affecting the local integration site sequence biases. These residues also determine the propensity of the virus to integrate into flexible tDNA sequences. Remarkably, natural polymorphisms INS119G and INR231G retarget viral integration away from gene dense regions, without affecting the interaction with the lentiviral tethering cofactor LEDGF/p75 (PSIP1). Precisely these variants were associated with rapid disease progression in a chronic HIV-1 subtype C infection cohort. These findings link integration site selection to virulence and viral evolution but also to the host immune response and antiretroviral therapy, since HIV-1 IN119 is under selection by HLA alleles and integrase inhibitors. LEDGF/p75 (PSIP1) ChIP-Seq using A300-848 antibody (recognizes p75 isoform) and input control in primary CD4+ T-cells
2015-01-26 | E-GEOD-61003 | biostudies-arrayexpress
Project description:Nucleocapsid (NC) CLIP-seq experiments were conducted on wild-type and eccentric HIV-1 virions generated in the presence of allosteric integrase inhibitor, BI-B2.
2017-06-15 | GSE100018 | GEO
Project description:The central nervous system encounters a number of challenges following HIV infection, leading to increased risk for a collection of neurocognitive symptoms clinically classified as HIV-associated neurocognitive disorders (HAND). Studies attempting to identify causal mechanisms and potential therapeutic interventions have historically relied on primary rodent neurons, but a number of recent reports take advantage of iPSC-derived neurons in order to study these mechanisms in a readily-reproducible, human model. We found that iPSC-derived neurons differentiated via an inducible neurogenin-2 transcription factor were resistant to gross toxicity from a number of HIV-associated insults previously reported to be toxic in rodent models, including HIV-infected myeloid cell supernatants and the integrase inhibitor antiretroviral drug, elvitegravir. Further examination of these cultures revealed robust resistance to NMDA receptor-mediated toxicity. We then performed a comparative analysis of iPSC neurons exposed to integrase inhibitors and activated microglial supernatants to study sub-cytotoxic alterations in micro electrode array (MEA)-measured neuronal activity and gene expression, identifying extracellular matrix interaction/morphogenesis as the most consistently altered pathways across HIV-associated insults. These findings illustrate that HIV-associated insults dysregulate human neuronal activity and organization even in the absence of gross NMDA-mediated neurotoxicity, which has important implications on the effects of these insults in neurodevelopment and on the interpretation of primary vs. iPSC in vitro neuronal studies.
2024-01-20 | GSE250609 | GEO
Project description:HIV-1 infection of human monocyte-derived dendritic cells with and without the integrase inhibitor, Raltegravir (gene expression).
| PRJNA391548 | ENA
Project description:HIV-1 infection of human monocyte-derived dendritic cells with and without the integrase inhibitor, Raltegravir (ATAC-Seq).
| PRJNA391485 | ENA