ArticleThe American journal of pathology2000
Induction of cell-cycle regulators in simian immunodeficiency virus encephalitis.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 63 citations in OpenAlex.
- 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
- Mechanisms of HIV-1 Tat neurotoxicity via CDK5 translocation and hyper-activation: role in HIV-associated neurocognitive disorders.Current HIV research · 2015Review
- 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
- Role of cell cycle re-entry in neurons: a common apoptotic mechanism of neuronal cell death.Neurotoxicity research · 2012Review
- Discrete phosphorylated retinoblastoma protein isoform expression in mouse tooth development.Journal of molecular histology · 2012Article
- Article
- Site-specific hyperphosphorylation of pRb in HIV-induced neurotoxicity.Molecular and cellular neurosciences · 2011Article
- E2F1 localizes predominantly to neuronal cytoplasm and fails to induce expression of its transcriptional targets in human immunodeficiency virus-induced neuronal damage.Neuroscience letters · 2010Article
- Article
- Retinoblastoma protein phosphorylation at multiple sites is associated with neurofibrillary pathology in Alzheimer disease.International journal of clinical and experimental pathology · 2008Article
- Human immunodeficiency virus infection inhibits granulocyte-macrophage colony-stimulating factor-induced microglial proliferation.Journal of neurovirology · 2007Article
- Location, location, location: altered transcription factor trafficking in neurodegeneration.Journal of neuropathology and experimental neurology · 2007Review
- Functional repression of cAMP response element in 6-hydroxydopamine-treated neuronal cells.The Journal of biological chemistry · 2006Article
- Human immunodeficiency virus type 1 genetic diversity in the nervous system: evolutionary epiphenomenon or disease determinant?Journal of neurovirology · 2005Review
- Regulation of cell cycle proteins by chemokine receptors: A novel pathway in human immunodeficiency virus neuropathogenesis?Journal of neurovirology · 2004Review
- The chemokine receptor CXCR4 regulates cell-cycle proteins in neurons.Journal of neurovirology · 2003Article
- Induction of pathogenic sets of genes in macrophages and neurons in NeuroAIDS.The American journal of pathology · 2003Article
- Cell cycle regulators in the neuronal death pathway of amyotrophic lateral sclerosis caused by mutant superoxide dismutase 1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Neuronal degeneration associated with human immunodeficiency virus encephalitis has been attributed to neurotoxicity of signaling molecules secreted by activated, infected macrophages. We hypothesized that the barrage of signals present in the extracellular milieu of human immunodeficiency virus-infiltrated brain causes inappropriate activation of neuronal cell-cycle machinery. We examined the presence of three members of the cell-cycle control machinery: pRb, E2F1, and p53 in the simian immunodeficiency virus encephalitis (SIVE) model. Compared to noninfected and simian immunodeficiency virus-infected, nonencephalitic controls, we observed increased protein expression of E2F1 and p53 and aberrant cellular localization of E2F1 and pRb. In SIVE, E2F1 was abundant in the cytoplasm of neurons in both neurons and astrocytes proximal to SIVE pathology in the basal ganglia. pRb staining was nuclear and cytoplasmic in cortical neurons of SIVE cases. Antibodies to phosphorylated pRb also labeled the cytoplasm of cortical neurons. These data suggest that in SIVE, cell signaling results in phosphorylation of pRb which may result in subsequent alteration in E2F1 activity. As increased E2F1 and p53 activities have been linked to cell death, these data suggest that the neurodegeneration in SIVE could in part be because of changes in expression and activity of cell-cycle machinery.
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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.