ArticlePloS one2013
Calcium/calcineurin synergizes with prostratin to promote NF-κB dependent activation of latent HIV.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- Article
- Network Pharmacology-Guided Identification ofInternational journal of molecular sciences · 2026Article
- Retinol Binding Protein 4 reactivates latent HIV-1 by triggering canonical NF-κB, JAK/STAT5 and JNK signalling.Signal transduction and targeted therapy · 2025Article
- Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal.eLife · 2025Article
- NSC95397 Is a Novel HIV-1 Latency-Reversing Agent.Viruses · 2024Article
- Release of P-TEFb from the Super Elongation Complex promotes HIV-1 latency reversal.PLoS pathogens · 2024Article
- NSC95397 is a Novel HIV-1 Latency Reversing Agent.bioRxiv : the preprint server for biology · 2024Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- Release of P-TEFb from the Super Elongation Complex promotes HIV-1 latency reversal.bioRxiv : the preprint server for biology · 2024Article
- The Impact of Spironolactone Co-administration on Cyclosporin Initial Dosage Optimization for Pediatric Refractory Nephrotic Syndrome.Current pharmaceutical design · 2024Article
- The hypoxia-regulated ectonucleotidase CD73 is a host determinant of HIV latency.Cell reports · 2023Article
- The role of tunneling nanotubes during early stages of HIV infection and reactivation: implications in HIV cure.NeuroImmune pharmacology and therapeutics · 2023Review
- The lysine methyltransferase SMYD5 amplifies HIV-1 transcription and is post-transcriptionally upregulated by Tat and USP11.Cell reports · 2023Article
- A modular CRISPR screen identifies individual and combination pathways contributing to HIV-1 latency.PLoS pathogens · 2023Article
- Droplet-microfluidics-assisted sequencing of HIV proviruses and their integration sites in cells from people on antiretroviral therapy.Nature biomedical engineering · 2022Article
- T cell stimulation remodels the latently HIV-1 infected cell population by differential activation of proviral chromatin.PLoS pathogens · 2022Article
- Article
- Natural killer cells induce HIV-1 latency reversal after treatment with pan-caspase inhibitors.Frontiers in immunology · 2022Article
- Fighting HIV-1 Persistence: At the Crossroads of "Shoc-K and B-Lock".Pathogens (Basel, Switzerland) · 2021Review
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Attempts to eradicate HIV have been thwarted by the persistence of a small pool of quiescent memory CD4 T cells that harbor a transcriptionally silent, integrated form of the virus that can produce infectious virions following an anamnestic immune response. Transcription factors downstream of T-cell receptor activation, such as NF-κB/Rel and nuclear factor of activated T cells (NFAT) transcription members, are considered important regulators of HIV transcription during acute HIV infection. We now report studies exploring their precise role as antagonists of HIV latency using cell and primary CD4 T cell models of HIV-1 latency. Surprisingly, RNA interference studies performed in J-Lat CD4 T cells suggested that none of the NFATs, including NFATc1, NFATc2, NFATc3, and NFAT5, played a key role in the reactivation of latent HIV. However, cyclosporin A markedly inhibited the reactivation response. These results were reconciled when calcium signaling through calcineurin was shown to potentiate prostratin induced activation of NF-κB that in turn stimulated the latent HIV long terminal repeat (LTR). Similar effects of calcineurin were confirmed in a primary CD4 T cell model of HIV latency. These findings highlight an important role for calcineurin in NF-κB-dependent induction of latent HIV transcription. Innovative approaches exploiting the synergistic actions of calcineurin and prostratin in the absence of generalized T-cell activation merit exploration as a means to attack the latent viral reservoir.
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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.