ArticleNeurochemical research2011
Neurodegenerative effects of recombinant HIV-1 Tat(1-86) are associated with inhibition of microtubule formation and oxidative stress-related reductions in microtubule-associated protein-2(a,b).
Article in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Stress granules at the crossroads of retroviral replication and antiviral immunity: mechanisms and therapeutic opportunities.Molecular biology reports · 2026Review
- Structural basis of microtubule depolymerization by the kinesin-like activity of HIV-1 Rev.Structure (London, England : 1993) · 2023Article
- Clathrin-nanoparticles deliver BDNF to hippocampus and enhance neurogenesis, synaptogenesis and cognition in HIV/neuroAIDS mouse model.Communications biology · 2022Article
- Article
- Hippocampal Up-Regulation of Apolipoprotein D in a Rat Model of Maternal Hypo- and Hyperthyroidism: Implication of Oxidative Stress.Neurochemical research · 2019Article
- HIV-associated neurodegeneration: exploitation of the neuronal cytoskeleton.Journal of neurovirology · 2019Review
- Neuroprotective effects of fatty acid amide hydrolase catabolic enzyme inhibition in a HIV-1 Tat model of neuroAIDS.Neuropharmacology · 2018Article
- Human Immunodeficiency Virus Promotes Mitochondrial Toxicity.Neurotoxicity research · 2017Review
- Role of Oxidative Stress in HIV-1-Associated Neurocognitive Disorder and Protection by Gene Delivery of Antioxidant Enzymes.Antioxidants (Basel, Switzerland) · 2014Review
- Ethanol impairs microtubule formation via interactions at a microtubule associated protein-sensitive site.Alcohol (Fayetteville, N.Y.) · 2013Article
- Infectious agents and neurodegeneration.Molecular neurobiology · 2012Review
- Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The human immunodeficiency virus 1 (HIV-1) protein Trans-activator of Transcription (Tat) is a nuclear regulatory protein that may contribute to the development of HIV-1 associated dementia by disrupting the neuronal cytoskeleton. The present studies examined effects of recombinant Tat(1-86; 1-100 nM) on microtubule-associated protein (MAP)-dependent and MAP-independent microtubule formation ex vivo and oxidative neuronal injury in rat organotypic hippocampal explants. Acute exposure to Tat(1-86) (≥1 nM) markedly reduced MAP-dependent and -independent microtubule formation ex vivo, as did vincristine sulfate (0.1-10 μM). Cytotoxicity, as measured by propidium iodide uptake, was observed in granule cells of the DG with exposure to 100 nM Tat(1-86) for 24 or 72 h, while significant reductions in MAP-2 immunoreactivity were observed in granule cells and pyramidal cells of the CA1 and CA3 regions at each timepoint. These effects were prevented by co-exposure to the soluble vitamin E analog Trolox (500 μM). Thus, effects of Tat(1-86) on the neuronal viability may be associated with direct interactions with microtubules and generation of oxidative stress.
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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.