ArticleJournal of cellular physiology2014
Neuroprotective activity of pDING in response to HIV-1 Tat.
Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Cloning of human DING: Developmental expression and downregulation by EtOH in-utero.Archives of internal medicine research · 2026Article
- Neurovirulent and non-neurovirulent strains of HIV-1 and their Tat proteins induce differential cytokine-chemokine profiles.NeuroImmune pharmacology and therapeutics · 2025Article
- Prenatal Alcohol Exposure Inhibits Transient Expression of Autophagy and Synaptic Proteins in Developing Brain.Obstetrics and gynecology research · 2025Article
- Article
- Effects of In Utero EtOH Exposure on 18S Ribosomal RNA Processing: Contribution to Fetal Alcohol Spectrum Disorder.International journal of molecular sciences · 2023Article
- Article
- Hypericum Genus as a Natural Source for Biologically Active Compounds.Plants (Basel, Switzerland) · 2022Review
- Gestational Age Variation in Human Placental Drug Transporters.Frontiers in pharmacology · 2022Article
- Fetal Brain Injury Models of Fetal Alcohol Syndrome: Examination of Neuronal Morphologic Condition Using Sholl Assay.Methods in molecular biology (Clifton, N.J.) · 2021Article
- DING Protein Inhibits Transcription of HIV-1 Gene through Suppression of Phosphorylation of NF-κB p65.Journal of HIV and AIDS · 2020Article
- HIV-1 and HIV-1-Tat Induce Mitochondrial DNA Damage in Human Neurons.Journal of HIV and AIDS · 2020Article
- HIV Protease Inhibitors Alter Amyloid Precursor Protein Processing via β-Site Amyloid Precursor Protein Cleaving Enzyme-1 Translational Up-Regulation.The American journal of pathology · 2017Article
- Targeting the Brain Reservoirs: Toward an HIV Cure.Frontiers in immunology · 2016Review
- HIV-1 Tat alters neuronal autophagy by modulating autophagosome fusion to the lysosome: implications for HIV-associated neurocognitive disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Creatine protects against mitochondrial dysfunction associated with HIV-1 Tat-induced neuronal injury.Current HIV research · 2014Article
- Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND).AIDS research and therapy · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although neurons are not productively infected with HIV-1, neuronal injury and death are frequently seen in the brains of AIDS patients with neurological and neurocognitive disorders. Evidently, viral proteins including Tat and cellular inflammatory factors released by activated and/or infected microglia, macrophages, and astrocytes contribute to neuronal cell death. Several studies have demonstrated that HIV-1 associated neuronal cell injury is mediated by dysregulation of signaling pathways that are controlled, in part, by a class of serine/threonine kinases. In this study, we demonstrate that pDING, a novel plant-derived phosphate binding protein has the capacity to reduce the severity of injury and death caused by HIV-1 and its neurotoxic Tat protein. We demonstrate that pDING, also called p27SJ/p38SJ, protects cells from the loss of neuronal processes induced by Tat and promotes neuronal outgrowth after Tat-mediated injury. Further, expression of pDING prevents Tat-induced oxidative stress and mitochondrial permeability. With its profound phosphatase activity, pDING controls the activity of several kinases including MAPK, Cdk5, and their downstream target protein, MEF2, which is implicated in neuronal cell protection. Our results show that expression of pDING in neuronal cells diminishes the level of hyperphosphorylated forms of Cdk5 and MEF2 caused by Tat and the other neurotoxic agents that are secreted by the HIV-1 infected cells. These observations suggest that pDING, through its phosphatase activity, has the ability to manipulate the state of phosphorylation and activity of several factors involved in neuronal cell health in response to HIV-1.
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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.