Evidence map›Paper›PMID 18521620›Full record

ArticleChromosoma2008

Plk1 regulates mitotic Aurora A function through betaTrCP-dependent degradation of hBora.

Eunice H Y Chan, Anna Santamaria, Herman H W Silljé, Erich A Nigg

Abstract read
In one paragraph

Article in Chromosoma, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

88 citing papers in PubMed.

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28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Eunice H Y ChanDepartment of Cell Biology, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Anna Santamaria
Herman H W Silljé
Erich A Nigg

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polo-like kinase 1 (Plk1) and Aurora A play key roles in centrosome maturation, spindle assembly, and chromosome segregation during cell division. Here we show that the functions of these kinases during early mitosis are coordinated through Bora, a partner of Aurora A first identified in Drosophila. Depletion of human Bora (hBora) results in spindle defects, accompanied by increased spindle recruitment of Aurora A and its partner TPX2. Conversely, hBora overexpression induces mislocalization of Aurora A and monopolar spindle formation, reminiscent of the phenotype seen in Plk1-depleted cells. Indeed, Plk1 regulates hBora. Following Cdk1-dependent recruitment, Plk1 triggers hBora destruction by phosphorylating a recognition site for SCF(Beta-TrCP). Plk1 depletion or inhibition results in a massive accumulation of hBora, concomitant with displacement of Aurora A from spindle poles and impaired centrosome maturation, but remarkably, co-depletion of hBora partially restores Aurora A localization and bipolar spindle formation. This suggests that Plk1 controls Aurora A localization and function by regulating cellular levels of hBora.

Indexed as

Amino Acid SequenceAnimalsAurora Kinase AAurora Kinasesbeta-Transducin Repeat-Containing ProteinsCell Cycle ProteinsCentrosomeGene SilencingHeLa CellsHumansMiceMitosisMolecular Sequence DataPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsAurka protein, mouseAurora Kinase AAurora Kinasesbeta-Transducin Repeat-Containing Proteinsbora protein, humanCell Cycle ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsRNA, Small InterferingSKP Cullin F-Box Protein Ligases

Identifiers

PMID18521620
PMCPMC2921497

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.