ArticleNeuroscience letters2010
E2F1 localizes predominantly to neuronal cytoplasm and fails to induce expression of its transcriptional targets in human immunodeficiency virus-induced neuronal damage.
Article in Neuroscience letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Exploring the Research Progress of Vascular Dementia and Key Regulatory Molecules: E2F1.International journal of molecular sciences · 2026Review
- Adaptations in Nucleus Accumbens Neuron Subtypes Mediate Negative Affective Behaviors in Fentanyl Abstinence.Biological psychiatry · 2023Article
- E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury.International journal of molecular sciences · 2022Article
- Identification and characterization of two novel alternatively spliced E2F1 transcripts in the rat CNS.Molecular and cellular neurosciences · 2018Article
- Review
- E2F1 in neurons is cleaved by calpain in an NMDA receptor-dependent manner in a model of HIV-induced neurotoxicity.Journal of neurochemistry · 2015Article
- HIV-1 gp120 and morphine induced oxidative stress: role in cell cycle regulation.Frontiers in microbiology · 2015Article
- Targeted gene mutation of E2F1 evokes age-dependent synaptic disruption and behavioral deficits.Journal of neurochemistry · 2014Article
- Antiretroviral drugs induce oxidative stress and neuronal damage in the central nervous system.Journal of neurovirology · 2014Article
- Calpain-mediated degradation of MDMx/MDM4 contributes to HIV-induced neuronal damage.Molecular and cellular neurosciences · 2013Article
- Chemotactic and mitogenic stimuli of neuronal apoptosis in patients with medically intractable temporal lobe epilepsy.Pathophysiology : the official journal of the International Society for Pathophysiology · 2013Article
- Activation status of integrated stress response pathways in neurones and astrocytes of HIV-associated neurocognitive disorders (HAND) cortex.Neuropathology and applied neurobiology · 2012Article
- Site-specific hyperphosphorylation of pRb in HIV-induced neurotoxicity.Molecular and cellular neurosciences · 2011Article
- The simian immunodeficiency virus targets central cell cycle functions through transcriptional repression in vivo.PloS one · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
As human immunodeficiency virus (HIV) does not induce neuronal damage by direct infection, the mechanisms of neuronal damage or loss in HIV-associated dementia (HAD) remain unclear. We have shown previously that immunoreactivity of transcription factor, E2F1, increases in neurons, localizing predominantly to the cytoplasm, in HIV-associated pathologies. Here we confirm that E2F1 localization is predominantly cytoplasmic in primary postmitotic neurons in vitro and cortical neurons in vivo. To determine whether E2F1 contributes to neuronal death in HAD via transactivation of target promoters, we assessed the mRNA and protein levels of several classical E2F1 transcriptional targets implicated in cell cycle progression and apoptosis in an in vitro model of HIV-induced neurotoxicity and in cortical autopsy tissue from patients infected with HIV. By Q-PCR, we show that mRNA levels of E2F1 transcriptional targets implicated in cell cycle progression (E2F1, Cyclin A, proliferating cell nuclear antigen (PCNA), and dyhydrofolate reductase (DHFR)) and apoptosis (caspases 3, 8, 9 and p19(ARF)) remain unchanged in an in vitro model of HIV-induced neurotoxicity. Further, we show that protein levels of p19(ARF), Cyclin A, and PCNA are not altered in vitro or in the cortex of patients with HAD. We propose that the predominantly cytoplasmic localization of E2F1 in neurons may account for the lack of E2F1 target transactivation in neurons responding to HIV-induced neurotoxicity.
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