ArticleJournal of neurovirology2007
Silencing the PTEN gene is protective against neuronal death induced by human immunodeficiency virus type 1 Tat.
Article in Journal of neurovirology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Silencing of PTEN inhibits the oxidative stress damage and hippocampal cell apoptosis induced by Sevoflurane through activating MEK1/ERK signaling pathway in infant rats.Cell cycle (Georgetown, Tex.) · 2020Article
- Role and mechanism of PTEN in Burkitt's lymphoma.Oncology reports · 2020Article
- Exosomal miR-9 Released from HIV Tat Stimulated Astrocytes Mediates Microglial Migration.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018Article
- NMDARs Adapt to Neurotoxic HIV Protein Tat Downstream of a GluN2A-Ubiquitin Ligase Signaling Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Incorporating the type and direction information in predicting novel regulatory interactions between HIV-1 and human proteins using a biclustering approach.BMC bioinformatics · 2014Article
- PTEN gene silencing prevents HIV-1 gp120(IIIB)-induced degeneration of striatal neurons.Journal of neurovirology · 2011Article
- Brain dysfunction in the era of combination antiretroviral therapy: implications for the treatment of the aging population of HIV-infected individuals.Current opinion in investigational drugs (London, England : 2000) · 2010Review
- Role of Tat protein in HIV neuropathogenesis.Neurotoxicity research · 2009Review
- BAG3 protein regulates caspase-3 activation in HIV-1-infected human primary microglial cells.Journal of cellular physiology · 2009Article
- Molecular epigenetics, chromatin, and NeuroAIDS/HIV: translational implications.Bioinformation · 2008Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Neurons are targets of toxicity induced by the human immunodeficiency virus (HIV)-1 protein Tat (transactivator of transcription). Exposure to Tat increases [Ca(2+)](i) in striatal neurons and activates multiple cell death pathways. In earlier studies the authors showed that Tat activated both caspase-3 and endonuclease-G, a caspase-independent effector of apoptosis, and that Tat-induced neurotoxicity was not attenuated by a caspase-3 inhibitor. Because Tat activates multiple, parallel death pathways, the authors attempted to reduce Tat-induced neurotoxicity by manipulating signaling pathways upstream of mitochondrial apoptotic events. PTEN (phosphatase and tensin homolog deleted on chromosome 10), a negative regulator of Akt/PKB (protein kinase B) phosphorylation, was chosen as a target for silencing. Akt/PKB activity directs multiple downstream pathways mediated by GSK3beta, BAD, forkhead transcription factors, nuclear factor kappa B (NFkappaB), and others, in a manner that promotes proliferation and survival. Striatal neurons were nucleofected with short interfering RNA (siRNA) vectors targeting PTEN, or a negative-control siRNA. Although Tat(1-86) significantly increased the death of neurons transfected with control construct by 72 h, PTEN-silenced neurons were completely protected. These findings indicate that Akt is a critical intermediary in the direct neurotoxicity induced by HIV-1 Tat, and identify Akt regulation as a possible therapeutic strategy for Tat-induced neurotoxicity in HIV encephalitis (HIVE).
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Registered trials
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