ReviewOncogene2005
Polo-like kinases in the nervous system.
Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 84 citations in OpenAlex.
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Conserved gene signatures shared amongFrontiers in molecular biosciences · 2023Article
- Tumor suppressor PLK2 may serve as a biomarker in triple-negative breast cancer for improved response to PLK1 therapeutics.Cancer research communications · 2021Article
- Three decades of Cdk5.Journal of biomedical science · 2021Review
- Transcriptome Remodeling in Gradual Development of Inverse Resistance between Paclitaxel and Cisplatin in Ovarian Cancer Cells.International journal of molecular sciences · 2020Article
- TNF-Mediated Homeostatic Synaptic Plasticity: FromFrontiers in cellular neuroscience · 2020Review
- Regulating a key mitotic regulator, polo-like kinase 1 (PLK1).Cytoskeleton (Hoboken, N.J.) · 2018Review
- Maternal immune activation alters brain microRNA expression in mouse offspring.Annals of clinical and translational neurology · 2018Article
- Lupus-Associated Functional Polymorphism in PNP Causes Cell Cycle Abnormalities and Interferon Pathway Activation in Human Immune Cells.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- Polo-like kinase 2 phosphorylation of amyloid precursor protein regulates activity-dependent amyloidogenic processing.Neuropharmacology · 2017Article
- Dissecting the Molecular Pathway Involved in PLK2 Kinase-mediated α-Synuclein-selective Autophagic Degradation.The Journal of biological chemistry · 2017Article
- Article
- Augmented expression of Polo-like kinase 1 is a strong predictor of shorter cancer-specific overall survival in early stage breast cancer at 15-year follow-up.Oncology letters · 2016Article
- Polo-Like Kinase 3 Appears Dispensable for Normal Retinal Development Despite Robust Embryonic Expression.PloS one · 2016Article
- Implication of Alpha-Synuclein Phosphorylation at S129 in Synucleinopathies: What Have We Learned in the Last Decade?Journal of Parkinson's disease · 2016Review
- Recent Advances and New Strategies in Targeting Plk1 for Anticancer Therapy.Trends in pharmacological sciences · 2015Review
- Prion-induced neurotoxicity: Possible role for cell cycle activity and DNA damage response.World journal of virology · 2015Review
- Current Update on Synopsis of miRNA Dysregulation in Neurological Disorders.CNS & neurological disorders drug targets · 2015Review
- Protein phosphorylation in neurodegeneration: friend or foe?Frontiers in molecular neuroscience · 2014Review
- Parkinson's disease-implicated kinases in the brain; insights into disease pathogenesis.Frontiers in molecular neuroscience · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo like kinases (Plks) are key regulators of the cell cycle, but little is known about their functions in postmitotic cells such as neurons. Recent findings indicate that Plk2 and Plk3 are dynamically regulated in neurons by synaptic activity at the mRNA and protein levels. In COS cells, Plk2 and Plk3 interact with spine-associated Rap guanosine triphosphatase-activating protein (SPAR), a regulator of actin dynamics and dendritic spine morphology, leading to its degradation through the ubiquitin-proteasome system. Induction of Plk2 in hippocampal neurons eliminates SPAR protein, depletes a core postsynaptic scaffolding molecule (PSD-95), and causes loss of mature dendritic spines and synapses. These findings implicate neuronal Plks as mediators of activity-dependent change in molecular composition and morphology of synapses. Induction of Plks might provide a homeostatic mechanism for global dampening of synaptic strength following heightened neuronal activity ('synaptic scaling'). Synapse-specific actions of induced Plks are also possible, particularly in light of the discovery of phosphoserine/threonine peptide motifs as binding targets of the polo box domain, which could allow for 'priming' phosphorylation by upstream kinases that could 'tag' Plk substrates only in specific synapses.
Indexed as
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What 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.