Evidence map›Paper›PMID 15923616›Full record

ArticleMolecular and cellular biology2005

Mechanism of Aurora-B degradation and its dependency on intact KEN and A-boxes: identification of an aneuploidy-promoting property.

Hao G Nguyen, Dharmaraj Chinnappan, Takeshi Urano, Katya Ravid

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
3.3field-weighted citation impact, top 8% of its field
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

78 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
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  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Aurora B Inhibitors as Cancer Therapeutics.Molecules (Basel, Switzerland) · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. APC/CJournal of cell science · 2020
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

18 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 at 2 institutions in 2 countries.

Hao G NguyenDepartment of Biochemistry, Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, K225, Boston, MA 02118, USA.
Dharmaraj Chinnappan
Takeshi Urano
Katya Ravid
Boston University · USNagoya University · JP

Funding

BIOLOGY OF THE LUNG--MULTIDISCIPLINARY PROGRAMT32HL007035 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Darrell N. Kotton, JOSEPH P MIZGERD · 1985 to 2026
$24.3M
NHLBI NIH HHS T32 HL007035NHLBI NIH HHS T32 HL07035PHS HHS 58537
6 · The paper itself

Abstract

The kinase Aurora-B, a regulator of chromosome segregation and cytokinesis, is highly expressed in a variety of tumors. During the cell cycle, the level of this protein is tightly controlled, and its deregulated abundance is suspected to contribute to aneuploidy. Here, we provide evidence that Aurora-B is a short-lived protein degraded by the proteasome via the anaphase-promoting cyclosome complex (APC/c) pathway. Aurora-B interacts with the APC/c through the Cdc27 subunit, Aurora-B is ubiquitinated, and its level is increased upon treatment with inhibitors of the proteasome. Aurora-B binds in vivo to the degradation-targeting proteins Cdh1 and Cdc20, the overexpression of which accelerates Aurora-B degradation. Using deletions or point mutations of the five putative degradation signals in Aurora-B, we show that degradation of this protein does not depend on its D-boxes (RXXL), but it does require intact KEN boxes and A-boxes (QRVL) located within the first 65 amino acids. Cells transfected with wild-type or A-box-mutated or KEN box-mutated Aurora-B fused to green fluorescent protein display the protein localized to the chromosomes and then to the midzone during mitosis, but the mutated forms are detected at greater intensities. Hence, we identified the degradation pathway for Aurora-B as well as critical regions for its clearance. Intriguingly, overexpression of a stable form of Aurora-B alone induces aneuploidy and anchorage-independent growth.

Indexed as

Amino Acid MotifsAneuploidyAnaphase-Promoting Complex-CyclosomeAnimalsAntineoplastic AgentsApc3 Subunit, Anaphase-Promoting Complex-CyclosomeAurora Kinase BAurora KinasesCdc20 ProteinsCell CycleCell Cycle ProteinsChromosomesCysteine Proteinase InhibitorsHeLa CellsHumansLeupeptinsAnaphase-Promoting Complex-CyclosomeAntineoplastic AgentsApc3 Subunit, Anaphase-Promoting Complex-CyclosomeAURKB protein, humanAurora Kinase BAurora Kinasesbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCDC20 protein, humanCdc20 ProteinsCDC27 protein, humanCell Cycle ProteinsCysteine Proteinase InhibitorsLeupeptinsNocodazoleProteasome Endopeptidase ComplexProteasome InhibitorsProtein Serine-Threonine KinasesRecombinant Fusion ProteinsUbiquitinUbiquitin-Protein Ligase Complexes

Identifiers

PMID15923616
PMCPMC1140599
OpenAlexW2155961719

What OpenQuestion holds

Textmetadata
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.