ArticleFrontiers in molecular neuroscience2017
Time-Dependent, HIV-Tat-Induced Perturbation of Human Neurons
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Transactivator of Transcription (Tat)-Induced Neuroinflammation as a Key Pathway in Neuronal Dysfunction: A Scoping Review.Molecular neurobiology · 2024Article
- Modulation of OPRM1 Alternative Splicing by Morphine and HIV-1 Nef.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Article
- Neuromodulation of BAG co-chaperones by HIV-1 viral proteins and HCell death discovery · 2021Article
- HIV-1C and HIV-1B Tat protein polymorphism in Southern Brazil.Journal of neurovirology · 2021Observational
- Neurocytoskeleton Proteins in Cerebrospinal Fluid of People With HIV-1 Subtypes B and C.Journal of acquired immune deficiency syndromes (1999) · 2020Article
- HIV-1 Tat alters neuronal intrinsic excitability.BMC research notes · 2018Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A significant proportion of human immunodeficiency virus type 1 (HIV)-positive individuals are affected by the cognitive, motor and behavioral dysfunction that characterizes HIV-associated neurocognitive disorders (HAND). While the molecular etiology of HAND remains largely uncharacterized, HIV transactivator of transcription (HIV-Tat) is thought to be an important etiological cause. Here we have used mass spectrometry (MS)-based discovery proteomics to identify the quantitative, cell-wide changes that occur when non-transformed, differentiated human neurons are treated with HIV-Tat over time. We identified over 4000 protein groups (false discovery rate <0.01) in this system with 131, 118 and 45 protein groups differentially expressed at 6, 24 and 48 h post treatment, respectively. Alterations in the expression of proteins involved in gene expression and cytoskeletal maintenance were particularly evident. In tandem with proteomic evidence of cytoskeletal dysregulation we observed HIV-Tat induced functional alterations, including a reduction of neuronal intrinsic excitability as assessed by patch-clamp electrophysiology. Our findings may be relevant for understanding
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