ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Cell cycle proteins exhibit altered expression patterns in lentiviral-associated encephalitis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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Who cites it
40 citing papers in PubMed, 74 citations in OpenAlex.
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- Neuronal Stress and Injury Caused by HIV-1, cART and Drug Abuse: Converging Contributions to HAND.Brain sciences · 2017Review
- Genomic integrity and the ageing brain.Nature reviews. Neuroscience · 2015Review
- E2F1 in neurons is cleaved by calpain in an NMDA receptor-dependent manner in a model of HIV-induced neurotoxicity.Journal of neurochemistry · 2015Article
- Mechanisms of HIV-1 Tat neurotoxicity via CDK5 translocation and hyper-activation: role in HIV-associated neurocognitive disorders.Current HIV research · 2015Review
- Multi-wavelength photoacoustic imaging of inducible tyrosinase reporter gene expression in xenograft tumors.Scientific reports · 2014Article
- Targeted gene mutation of E2F1 evokes age-dependent synaptic disruption and behavioral deficits.Journal of neurochemistry · 2014Article
- Microglial derived tumor necrosis factor-α drives Alzheimer's disease-related neuronal cell cycle events.Neurobiology of disease · 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
- Podocyte mitosis - a catastrophe.Current molecular medicine · 2013Review
- Role of cell cycle re-entry in neurons: a common apoptotic mechanism of neuronal cell death.Neurotoxicity research · 2012Review
- Parallel high throughput neuronal toxicity assays demonstrate uncoupling between loss of mitochondrial membrane potential and neuronal damage in a model of HIV-induced neurodegeneration.Neuroscience research · 2011Article
- Site-specific hyperphosphorylation of pRb in HIV-induced neurotoxicity.Molecular and cellular neurosciences · 2011Article
- Survivin mutant protects differentiated dopaminergic SK-N-SH cells against oxidative stress.PloS one · 2011Article
- HIV-associated neurocognitive disorder: pathogenesis and therapeutic opportunities.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Cell cycle proteins regulate processes as diverse as cell division and cell death. Recently their role in neuronal death has been reported in several models of neurodegeneration. We have reported previously that two key regulators of the cell cycle, the retinoblastoma susceptibility gene product (pRb) and transcription factor E2F1, exhibit altered immunostaining patterns in simian immunodeficiency virus encephalitis (SIVE). Here we show that E2F1 and the inactivated, hyperphosphorylated form of pRb (ppRb) also exhibit altered immunostaining patterns in human immunodeficiency virus encephalitis (HIVE). Quantification of E2F1 and ppRb staining by immunofluorescent confocal microscopy confirms a significant increase in E2F1 and ppRb in both HIVE and the simian model. This increase in E2F1 and ppRb staining correlates with an increase in the presence of activated macrophages, suggesting a link between changes in cell cycle proteins and the presence of activated macrophages. Changes in ppRb and E2F1 staining in SIVE also correlate with alterations in E2F/DNA binding complexes present in the nuclear and cytoplasmic fractions from both midfrontal cortex and basal ganglia. These findings suggest that changes in cell cycle proteins occur in both HIVE and the simian model and that these changes have functional implications for gene expression in neural cells under encephalitic conditions mediated by macrophage activation or infiltration.
Indexed as
Identifiers
11896158PMC3670958W1962365951What OpenQuestion holds
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.