ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Two-pore channels regulate Tat endolysosome escape and Tat-mediated HIV-1 LTR transactivation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 39 citations in OpenAlex.
- Targeting virus-interacting host ion channels as a novel antiviral strategy.Acta pharmacologica Sinica · 2026Review
- HERV-K (HML-2) Envelope Protein Induces Mitochondrial Depolarization and Neurotoxicity via Endolysosome Iron Dyshomeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- HIV-1 Tat Induces Dysregulation of PGC1-Alpha and Sirtuin 3 Expression in Neurons: The Role of Mitochondrial Biogenesis in HIV-Associated Neurocognitive Disorder (HAND).International journal of molecular sciences · 2023Article
- NAADP-Mediated CaHandbook of experimental pharmacology · 2023Article
- Two-pore channels: going with the flows.Biochemical Society transactions · 2022Article
- The ins and outs of virus trafficking through acidic CaCell calcium · 2022Review
- NAADP-binding proteins find their identity.Trends in biochemical sciences · 2022Review
- HIV-1 Tat endocytosis and retention in endolysosomes affects HIV-1 Tat-induced LTR transactivation in astrocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Sirtuins Modulation: A Promising Strategy for HIV-Associated Neurocognitive Impairments.International journal of molecular sciences · 2022Review
- Targeting the two-pore channel 2 in cancer progression and metastasis.Exploration of targeted anti-tumor therapy · 2022Review
- Review
- Endolysosome iron restricts Tat-mediated HIV-1 LTR transactivation by increasing HIV-1 Tat oligomerization and β-catenin expression.Journal of neurovirology · 2021Article
- Review
- Review
- Lysosomal Stress Response (LSR): Physiological Importance and Pathological Relevance.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Review
- Pharmacological Modulators of Autophagy as a Potential Strategy for the Treatment of COVID-19.International journal of molecular sciences · 2021Review
- Essential requirement for JPT2 in NAADP-evoked CaScience signaling · 2021Article
- Time-Dependent Internalization of S100B by Mesenchymal Stem CellsFrontiers in cell and developmental biology · 2021Article
- Overcoming Chemoresistance: Altering pH of Cellular Compartments by Chloroquine and Hydroxychloroquine.Frontiers in cell and developmental biology · 2021Review
- Possible Therapeutic Use of Natural Compounds Against COVID-19.Journal of cellular signaling · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
HIV-1 Tat is essential for HIV-1 replication and appears to play an important role in the pathogenesis of HIV-associated neurological complications. Secreted from infected or transfected cells, Tat has the extraordinary ability to cross the plasma membrane. In the brain, Tat can be taken up by CNS cells via receptor-mediated endocytosis. Following endocytosis and its internalization into endolysosomes, Tat must be released in order for it to activate the HIV-1 LTR promoter and facilitate HIV-1 viral replication in the nucleus. However, the underlying mechanisms whereby Tat escapes endolysosomes remain unclear. Because Tat disrupts intracellular calcium homeostasis, we investigated the involvement of calcium in Tat endolysosome escape and subsequent LTR transactivation. We demonstrated that chelating endolysosome calcium with high-affinity rhodamine-dextran or chelating cytosolic calcium with BAPTA-AM attenuated Tat endolysosome escape and LTR transactivation. Significantly, we demonstrated that pharmacologically blocking and knocking down the endolysosome-resident two-pore channels (TPCs) attenuated Tat endolysosome escape and LTR transactivation. This calcium-mediated effect appears to be selective for TPCs because knocking down TRPML1 calcium channels was without effect. Our findings suggest that calcium released from TPCs is involved in Tat endolysosome escape and subsequent LTR transactivation. TPCs might represent a novel therapeutic target against HIV-1 infection and HIV-associated neurological complications.
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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.