ArticleCell cycle (Georgetown, Tex.)2008
Involvement of the p53 and p73 transcription factors in neuroAIDS.
Article in Cell cycle (Georgetown, Tex.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- HIV-1-related factors interact with p53 to influence cellular processes.AIDS research and therapy · 2023Review
- HIV-1 Tat protein promotes neuronal dysregulation by inhibiting E2F transcription factor 3 (E2F3).The Journal of biological chemistry · 2019Article
- Network analysis of hippocampal neurons by microelectrode array in the presence of HIV-1 Tat and cocaine.Journal of cellular physiology · 2018Article
- HIV-1 Viral Protein R Activates NLRP3 Inflammasome in Microglia: implications for HIV-1 Associated Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- HIV-1 Tat and Cocaine Impair Survival of Cultured Primary Neuronal Cells via a Mitochondrial Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Article
- Role of the immune system in HIV-associated neuroinflammation and neurocognitive implications.Brain, behavior, and immunity · 2015Review
- p53 as a retrovirus-induced oxidative stress modulator.The Journal of general virology · 2015Article
- Roles and functions of HIV-1 Tat protein in the CNS: an overview.Virology journal · 2013Review
- HIV Associated Neurocognitive Disorders.Infectious disease reports · 2013Review
- Article
- Role of p53 in neurodegenerative diseases.Neuro-degenerative diseases · 2012Review
- HIV-1 Tat protein promotes neuronal dysfunction through disruption of microRNAs.The Journal of biological chemistry · 2011Article
- Mitogen-activated protein kinase p38 in HIV infection and associated brain injury.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Review
- High-performance capillary electrophoresis for determining HIV-1 Tat protein in neurons.PloS one · 2011Article
- HIV-1 associated dementia: update on pathological mechanisms and therapeutic approaches.Current opinion in neurology · 2009Review
- Polyamines: Predictive Biomarker for HIV-Associated Neurocognitive Disorders.Journal of AIDS & clinical researchArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
HIV-associated dementia (HAD) is the most common AIDS-associated neurological disorder and is characterized by the development of synaptodendritic injury to neurons. To advance HAD therapy, it is crucial to identify the mechanisms and factors involved. The viral protein HIV-1 Tat is among those factors and is released by HIV-1-infected cells and can be taken up by adjacent neuronal cells leading to neurotoxic effects. Multiple cellular host proteins have been identified as Tat cofactors in causing neuronal injury. Interestingly, most of these factors function through activation of the p53 pathway. We have now examined the ability of Tat to activate the p53 pathway leading to the induction of endogenous p53 and p73 in neuronal cells. We found that Tat induced p53 and p73 levels in SH-SY5Y cells and that this induction caused retraction of neurites. In the absence of either p53 or p73, Tat failed to induce dendritic retraction or to activate the proapoptotic proteins, such as Bax. Further, we found that p53-accumulation in Tat-treated cells depends on the presence of p73. Therefore, we conclude that Tat contributes to neuronal degeneration through activation of a pathway involving p53 and p73. This information will be valuable for the development of therapeutic agents that affect these pathways to protect CNS neurons and prevent HAD.
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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.