ArticleJournal of molecular biology2011
ESCRT machinery potentiates HIV-1 utilization of the PI(4,5)P(2)-PLC-IP3R-Ca(2+) signaling cascade.
Article in Journal of molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Dysregulation of host cell calcium signaling during viral infections: Emerging paradigm with high clinical relevance.Molecular aspects of medicine · 2021Review
- Structural insight into host plasma membrane association and assembly of HIV-1 matrix protein.Scientific reports · 2021Article
- Pharmic Activation of PKG2 Alleviates Diabetes-Induced Osteoblast Dysfunction by Suppressing PLCOxidative medicine and cellular longevity · 2021Article
- Review
- Review
- HIV-1 intron-containing RNA expression induces innate immune activation and T cell dysfunction.Nature communications · 2018Article
- Notoginsenoside R1 Alleviates Oxygen-Glucose Deprivation/Reoxygenation Injury by Suppressing Endoplasmic Reticulum Calcium Release via PLC.Scientific reports · 2017Article
- Structure, functional regulation and signaling properties of Rap2B.Oncology letters · 2016Article
- Calcium Regulation of Hemorrhagic Fever Virus Budding: Mechanistic Implications for Host-Oriented Therapeutic Intervention.PLoS pathogens · 2015Article
- PIP2: choreographer of actin-adaptor proteins in the HIV-1 dance.Trends in microbiology · 2014Review
- Tsg101 regulates PI(4,5)P2/Ca(2+) signaling for HIV-1 Gag assembly.Frontiers in microbiology · 2014Article
- Double-membraned liposomes sculpted by poliovirus 3AB protein.The Journal of biological chemistry · 2013Article
- 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
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) release efficiency is directed by late (L) domain motifs in the viral structural precursor polyprotein Gag, which serve as links to the ESCRT (endosomal sorting complex required for transport) machinery. Linkage is normally through binding of Tsg101, an ESCRT-1 component, to the P(7)TAP motif in the p6 region of Gag. In its absence, budding is directed by binding of Alix, an ESCRT adaptor protein, to the LY(36)PX(n)L motif in Gag. We recently showed that budding requires activation of the inositol 1,4,5-triphosphate receptor (IP3R), a protein that "gates" Ca(2+) release from intracellular stores, triggers Ca(2+) cell influx and thereby functions as a major regulator of Ca(2+) signaling. In the present study, we determined whether the L domain links Gag to Ca(2+) signaling machinery. Depletion of IP3R and inactivation of phospholipase C (PLC) inhibited budding whether or not Tsg101 was bound to Gag. PLC hydrolysis of phosphatidylinositol-(4,5)-bisphosphate generates inositol (1,4,5)-triphosphate, the ligand that activates IP3R. However, with Tsg101 bound, Gag release was independent of Gq-mediated activation of PLC, and budding was readily enhanced by pharmacological stimulation of PLC. Moreover, IP3R was redistributed to the cell periphery and cytosolic Ca(2+) was elevated, events indicative of induction of Ca(2+) signaling. The results suggest that L domain function, ESCRT machinery and Ca(2+) signaling are linked events in Gag release.
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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.