ArticleJournal of neuropathology and experimental neurology2011
The cell cycle regulator phosphorylated retinoblastoma protein is associated with tau pathology in several tauopathies.
Article in Journal of neuropathology and experimental neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Alzheimer's disease and related tauopathies: disorders of disrupted neuronal identity.Trends in neurosciences · 2023Review
- Functional variants identify sex-specific genes and pathways in Alzheimer's Disease.Nature communications · 2023Article
- Neuronal Cell Cycle Re-Entry Enhances Neuropathological Features in AppNLF Knock-In Mice.Journal of Alzheimer's disease : JAD · 2021Article
- Genotoxic Damage During Brain Development Presages Prototypical Neurodegenerative Disease.Frontiers in neuroscience · 2021Review
- Commentary on Singh et al. (2020) Postzygotic Somatic Mutations in the Human Brain Expand the Threshold-Liability Model of Schizophrenia.Frontiers in psychiatry · 2021Article
- Core cell cycle machinery is crucially involved in both life and death of post-mitotic neurons.Cellular and molecular life sciences : CMLS · 2020Review
- High S phase kinase-associated protein 2 expression is a potential prognostic biomarker for glioma.Oncology letters · 2020Article
- Iron Oxide Nanoparticles Induces Cell Cycle-Dependent Neuronal Apoptosis in Mice.Journal of molecular neuroscience : MN · 2018Article
- Increased Wnt Signaling and Reduced Viability in a Neuronal Model of Progranulin-Deficient Frontotemporal Lobar Degeneration.Molecular neurobiology · 2016Article
- Distinct chronology of neuronal cell cycle re-entry and tau pathology in the 3xTg-AD mouse model and Alzheimer's disease patients.Journal of Alzheimer's disease : JAD · 2015Article
- Article
- MiR-26b, upregulated in Alzheimer's disease, activates cell cycle entry, tau-phosphorylation, and apoptosis in postmitotic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Phosphorylated retinoblastoma protein (p-Rb) is involved in neuronal apoptosis after traumatic brain injury in adult rats.Journal of molecular histology · 2013Article
- Deferiprone reduces amyloid-β and tau phosphorylation levels but not reactive oxygen species generation in hippocampus of rabbits fed a cholesterol-enriched diet.Journal of Alzheimer's disease : JAD · 2012Article
- The expression of retinoblastoma tumor suppressor protein in oral cancers and precancers: A clinicopathological study.Dental research journalArticle
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Retinoblastoma protein (pRb) is a ubiquitous 928-amino acid cell cycle regulatory molecule with diverse biologic activities. One critical function of pRb is the control of the G1-to-S phase checkpoint of the cell cycle. In the hypophosphorylated state, pRb suppresses the activity of E2F transcription factors thereby inhibiting transcription of cell cycle-promoting genes. On phosphorylation, primarily by cyclin-dependent kinases, phosphorylated pRb dissociates from E2F and permits cell cycle progression. We previously found phosphorylated pRb to be intimately associated with hyperphosphorylated tau-containing neurofibrillary tangles of Alzheimer disease (AD), the pathogenesis of which is believed to involve dysregulation of the cell cycle and marked neuronal death. Here, we used immunohistochemistry to investigate the presence of phosphorylated pRb in other distinct neurodegenerative diseases that share the common characteristic of hyperphosphorylated tau pathology and neuronal loss with AD.We found colocalized labeling of tau pathology and phosphorylated pRb in Pick disease and progressive supranuclear palsy (3 cases each), neurodegeneration with brain iron accumulation type 1 (2 cases), and Parkinson-amyotrophic lateral sclerosis of Guam, subacute sclerosing panencephalitis, frontotemporal dementia and Parkinsonism linked to chromosome 17, and dementia pugilistica (1 case each). These observations further implicate aberrant neuronal cell cycle progression in neurodegenerative diseases, particularly tauopathies, and suggest a novel target for therapeutic intervention.
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