ArticleOncogene2008
Aurora-A and ch-TOG act in a common pathway in control of spindle pole integrity.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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
39 citing papers in PubMed, 63 citations in OpenAlex.
- Meiotic progression in multinuclear mouse spermatocytes without the spindle pole clustering motor protein KIFC1 or cytokinesis forms single-cell late-stage spermatids.Scientific reports · 2025Article
- Aurora kinases signaling in cancer: from molecular perception to targeted therapies.Molecular cancer · 2025Review
- Review
- Spermatocytes have the capacity to segregate chromosomes despite centriole duplication failure.EMBO reports · 2024Article
- Male meiotic spindle poles are stabilized by TACC3 and cKAP5/chTOG differently from female meiotic or somatic mitotic spindles in mice.Scientific reports · 2024Article
- The GCN2/eIF2αK stress kinase regulates PP1 to ensure mitotic fidelity.EMBO reports · 2023Article
- Therapeutic gene silencing ofScience advances · 2023Article
- TACC3-ch-TOG interaction regulates spindle microtubule assembly by controlling centrosomal recruitment of γ-TuRC.Bioscience reports · 2023Article
- Review
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Identification and characterization of deschloro-chlorothricin obtained from a large natural product library targeting aurora A kinase in multiple myeloma.Investigational new drugs · 2021Article
- Aurora A Protein Kinase: To the Centrosome and Beyond.Biomolecules · 2019Review
- The functional diversity of Aurora kinases: a comprehensive review.Cell division · 2018Review
- A centrosomal protein STARD9 promotes microtubule stability and regulates spindle microtubule dynamics.Cell cycle (Georgetown, Tex.) · 2018Article
- A FRET biosensor reveals spatiotemporal activation and functions of aurora kinase A in living cells.Nature communications · 2016Article
- Aurora A's Functions During Mitotic Exit: The Guess Who Game.Frontiers in oncology · 2015Review
- Aurora A inhibition by MNL8054 promotes centriole elongation during Drosophila male meiosis.Cell cycle (Georgetown, Tex.) · 2015Article
- AIBp regulates mitotic entry and mitotic spindle assembly by controlling activation of both Aurora-A and Plk1.Cell cycle (Georgetown, Tex.) · 2015Article
- The Aurora-A inhibitor MLN8237 affects multiple mitotic processes and induces dose-dependent mitotic abnormalities and aneuploidy.Oncotarget · 2014Article
- Mitotic spindle multipolarity without centrosome amplification.Nature cell biology · 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
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitotic spindle assembly is a highly regulated process, crucial to ensure the correct segregation of duplicated chromosomes in daughter cells and to avoid aneuploidy, a common feature of tumors. Among the most important spindle regulators is Aurora-A, a mitotic centrosomal kinase frequently overexpressed in tumors. Here, we investigated the role of Aurora-A in spindle pole organization in human cells. We show that RNA interference-mediated Aurora-A inactivation causes pericentriolar material fragmentation in prometaphase, yielding the formation of spindles with supernumerary poles. This fragmentation does not necessarily involve centrioles and requires microtubules (MTs). Aurora-A-depleted prometaphases mislocalize the MT-stabilizing protein colonic hepatic tumor-overexpressed gene (ch-TOG), which abnormally accumulates at spindle poles, as well as the mitotic centromere-associated kinesin (MCAK), the major functional antagonist of ch-TOG, which delocalizes from poles. ch-TOG is required for extrapole formation in prometaphases lacking Aurora-A, because co-depletion of Aurora-A and ch-TOG mitigates the fragmented pole phenotype. These results indicate a novel function of Aurora-A, the regulation of ch-TOG and MCAK localization, and highlight a common pathway involving the three factors in control of spindle pole integrity.
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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.