Evidence map›Paper›PMID 27332895›Full record

ArticlePloS one2016

Aurora-C Interactions with Survivin and INCENP Reveal Shared and Distinct Features Compared with Aurora-B Chromosome Passenger Protein Complex.

Kaori Sasai, Hiroshi Katayama, David H Hawke, Subrata Sen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

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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 1 institution in 1 country.

Kaori SasaiDepartment of Translational Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Houston, Texas, United States of America.
Hiroshi KatayamaDepartment of Translational Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Houston, Texas, United States of America.
David H HawkeDepartment of Systems Biology, University of Texas M.D. Anderson Cancer Center, Houston, Texas, United States of America.
Subrata SenDepartment of Translational Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Houston, Texas, United States of America.
The University of Texas MD Anderson Cancer Center · US

Funding

Novel human oncogene STK15/BTAK/Aurora 2R01CA089716 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SEN, SUBRATA · 2001 to 2012
$2.3M
NCI NIH HHS R01 CA089716
6 · The paper itself

Abstract

Aurora-C, a member of the Aurora kinase family that can complement Aurora-B function in mitosis is either moderately expressed or repressed in most adult somatic tissues but is active in early embryonic development and expressed at elevated levels in multiple human cancers. Aurora-C overexpression reportedly plays a role in tumorigenic transformation. We performed detailed characterization of Aurora-C interactions with members of the Chromosome Passenger Complex (CPC), Survivin and Inner Centromere Protein (INCENP) in reference to known Aurora-B interactions to understand the functional significance of Aurora-C overexpression in human cancer cells. The results revealed that silencing of Aurora-C or -B individually does not affect localization of the other kinase and the two kinases exist predominantly in independent complexes in vivo. Presence of Aurora-C and -B in molecular complexes of varying as well as overlapping sizes and co-existence in INCENP overexpressing cells indicated oligomerization of ternary complexes under different physiological conditions in vivo. Furthermore, Aurora-C and -B stabilized INCENP through interaction with and phosphorylation of the IN box domain while Aurora-C was activated following Survivin phosphorylation on Serine 20. Phosphorylation of Survivin residue Serine 20 by Aurora-C and -B appears important for proper chromosome segregation. Taken together, our study suggests that Aurora-C, expressed at low levels in somatic cells, functions as a catalytic component of the CPC together with Aurora-B through mitosis. Elevated expression of Aurora-C in cancer cells alters the structural and functional characteristics of the Aurora-B-CPC leading to chromosomal instability.

Indexed as

Amino Acid SequenceAurora Kinase BAurora Kinase CCentrifugation, Density GradientChromosomal Proteins, Non-HistoneChromosome SegregationConserved SequenceCytokinesisGene SilencingHeLa CellsHumansImmunoprecipitationInhibitor of Apoptosis ProteinsModels, BiologicalPhosphorylationPhosphoserineAurora Kinase BAurora Kinase CBIRC5 protein, humanChromosomal Proteins, Non-HistoneINCENP protein, humanInhibitor of Apoptosis ProteinsPhosphoserineSurvivin

Identifiers

PMID27332895
PMCPMC4917241
OpenAlexW2468063196

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Registered trials

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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.