ArticleJournal of virology2010
Activation of the inositol (1,4,5)-triphosphate calcium gate receptor is required for HIV-1 Gag release.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting virus-interacting host ion channels as a novel antiviral strategy.Acta pharmacologica Sinica · 2026Review
- A novel antiviral strategy by disrupting the equilibrium of virus-host calcium homeostasis.Current opinion in virology · 2026Review
- Dysregulation of host cell calcium signaling during viral infections: Emerging paradigm with high clinical relevance.Molecular aspects of medicine · 2021Review
- Review
- Opportunistic intruders: how viruses orchestrate ER functions to infect cells.Nature reviews. Microbiology · 2016Review
- Identification of Host Cell Factors Associated with Astrovirus Replication in Caco-2 Cells.Journal of virology · 2015Article
- Parallel epigenomic and transcriptomic responses to viral infection in honey bees (Apis mellifera).PLoS pathogens · 2015Article
- Role of Gag and lipids during HIV-1 assembly in CD4(+) T cells and macrophages.Frontiers in microbiology · 2014Review
- Integration of modeling with experimental and clinical findings synthesizes and refines the central role of inositol 1,4,5-trisphosphate receptor 1 in spinocerebellar ataxia.Frontiers in neuroscience · 2014Review
- Tsg101 regulates PI(4,5)P2/Ca(2+) signaling for HIV-1 Gag assembly.Frontiers in microbiology · 2014Article
- The S40 residue in HIV-1 Gag p6 impacts local and distal budding determinants, revealing additional late domain activities.Retrovirology · 2013Article
- Article
- Defective HIV-1 particle assembly in AP-3-deficient cells derived from patients with Hermansky-Pudlak syndrome type 2.Journal of virology · 2012Article
- HIV Assembly and Budding: Ca(2+) Signaling and Non-ESCRT Proteins Set the Stage.Molecular biology international · 2012Article
- ESCRT machinery potentiates HIV-1 utilization of the PI(4,5)P(2)-PLC-IP3R-Ca(2+) signaling cascade.Journal of molecular biology · 2011Article
- Evidence of a role for soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) machinery in HIV-1 assembly and release.The Journal of biological chemistry · 2011Article
- New insights into HIV assembly and trafficking.Physiology (Bethesda, Md.) · 2011Review
- Sprouty2 regulates PI(4,5)P2/Ca2+ signaling and HIV-1 Gag release.Journal of molecular biology · 2011Article
- Molecular determinants that regulate plasma membrane association of HIV-1 Gag.Journal of molecular biology · 2011Review
- Inositol 1,4,5-trisphosphate receptor subtype-specific regulation of calcium oscillations.Neurochemical research · 2011Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The structural precursor polyprotein, Gag, encoded by all retroviruses, including the human immunodeficiency virus type 1 (HIV-1), is necessary and sufficient for the assembly and release of particles that morphologically resemble immature virus particles. Previous studies have shown that the addition of Ca(2+) to cells expressing Gag enhances virus particle production. However, no specific cellular factor has been implicated as mediator of Ca(2+) provision. The inositol (1,4,5)-triphosphate receptor (IP3R) gates intracellular Ca(2+) stores. Following activation by binding of its ligand, IP3, it releases Ca(2+) from the stores. We demonstrate here that IP3R function is required for efficient release of HIV-1 virus particles. Depletion of IP3R by small interfering RNA, sequestration of its activating ligand by expression of a mutated fragment of IP3R that binds IP3 with very high affinity, or blocking formation of the ligand by inhibiting phospholipase C-mediated hydrolysis of the precursor, phosphatidylinositol-4,5-biphosphate, inhibited Gag particle release. These disruptions, as well as interference with ligand-receptor interaction using antibody targeted to the ligand-binding site on IP3R, blocked plasma membrane accumulation of Gag. These findings identify IP3R as a new determinant in HIV-1 trafficking during Gag assembly and introduce IP3R-regulated Ca(2+) signaling as a potential novel cofactor in viral particle release.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.