Evidence map›Paper›PMID 23095493›Full record

ArticleCell cycle (Georgetown, Tex.)2012

FBXW7 is involved in Aurora B degradation.

Chieh-Lin Teng, Yun-Chi Hsieh, Liem Phan, Jihyun Shin, Chris Gully, Guermarie Velazquez-Torres, Stephen Skerl, Sai-Ching J Yeung, Shih-Lan Hsu, Mong-Hong Lee

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. BRD4 regulates Aurora B kinase activity.bioRxiv : the preprint server for biology · 2025
    Article
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  12. Review
  13. Tumor Suppressor FBXW7 and Its Regulation of DNA Damage Response and Repair.Frontiers in cell and developmental biology · 2021
    Review
  14. Article
  15. Article
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  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 3 countries.

Chieh-Lin TengDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Yun-Chi Hsieh
Liem Phan
Jihyun Shin
Chris Gully
Guermarie Velazquez-Torres
Stephen Skerl
Sai-Ching J Yeung
Shih-Lan Hsu
Mong-Hong Lee
The University of Texas MD Anderson Cancer Center · USTaichung Veterans General Hospital · TWCentre for Cancer Biology · AU

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
R25 SUPPLEMENT IN GENETIC EPIDEMIOLOGY EDUCATIONR25CA057730 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CHANG, SHINE · 1992 to 2016
$18.6M
Regulation of cyclin-dependent kinase inhibitor p27 in cancerR01CA089266 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MONG-HONG · 2002 to 2013
$2.8M
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA089266NCI NIH HHS R01CA089266NCI NIH HHS R25 CA057730NCI NIH HHS R25T CA57730
6 · The paper itself

Abstract

FBXW7, a component of E3 ubiquitin ligase, plays an important role in mitotic checkpoint, but its role remains unclear. Aurora B is a mitotic checkpoint kinase that plays a pivotal role in mitosis by ensuring correct chromosome segregation and normal progression through mitosis. Whether Aurora B and FBXW7 are coordinately regulated during mitosis is not known. Here, we show that FBXW7 is a negative regulator for Aurora B. Ectopic expression of FBXW7 can suppress the expression of Aurora B. Accordingly, FBXW7 deficiency leads to Aurora B elevation. Mechanistic studies show that all FBXW7 isoforms are negative regulators of Aurora B expression through ubiquitination-mediated protein degradation. Aurora B interacts with R465 and R505 residues of WD 40 domain of FBXW7. Significantly, inverse correlation between FBXW7 and Aurora B elevation is translated into the deregulation of mitosis. FBWX7 expression mitigates Aurora B-mediated cell growth and mitotic deregulation. In addition, FBXW7 reduces the percentage of multinucleated cells caused by Aurora B overexpression. These data suggest that FBXW7 is an important negative regulator of Aurora B, and that the loss or mutation of FBXW7 as seen in many types of cancer could lead to an abnormal elevation of Aurora B and result in deregulated mitosis, which accelerates cancer cell growth.

Indexed as

Aurora Kinase BAurora KinasesCell Cycle ProteinsCell ProliferationF-Box ProteinsF-Box-WD Repeat-Containing Protein 7HCT116 CellsHEK293 CellsHumansLeupeptinsMitosisProtease InhibitorsProtein BindingProtein IsoformsProtein Serine-Threonine KinasesProtein StabilityAURKB protein, humanAurora Kinase BAurora Kinasesbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCell Cycle ProteinsF-Box ProteinsF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanLeupeptinsProtease InhibitorsProtein IsoformsProtein Serine-Threonine KinasesUbiquitin-Protein Ligases

Identifiers

PMID23095493
PMCPMC3507501
OpenAlexW2086286750

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.