Evidence map›Paper›PMID 28202658›Full record

ReviewBiochemical Society transactions2017

Mechanisms for nonmitotic activation of Aurora-A at cilia.

Vladislav Korobeynikov, Alexander Y Deneka, Erica A Golemis

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2017. 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
3.5field-weighted citation impact, top 7% 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, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Primary cilia and neural computation.Journal of biomedical science · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Patterns of Ciliation and Ciliary Signaling in Cancer.Reviews of physiology, biochemistry and pharmacology · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Targeting E3 Ubiquitin Ligases and Deubiquitinases in Ciliopathy and Cancer.International journal of molecular sciences · 2020
    Review
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Vladislav KorobeynikovMolecular Therapeutics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, U.S.A.
Alexander Y DenekaMolecular Therapeutics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, U.S.A.
Erica A GolemisMolecular Therapeutics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, U.S.A. erica.golemis@fccc.edu.
Kazan Federal University · RU

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Dietmar J Kappes · 1985 to 2026
$138.8M
Interaction of protein-targeted therapeutics and ciliary dynamicsR01DK108195 · NIDDK · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 2016 to 2020
$2.0M
NCI NIH HHS P30 CA006927NIDDK NIH HHS R01 DK108195
6 · The paper itself

Abstract

Overexpression of the Aurora kinase A (AURKA) is oncogenic in many tumors. Many studies of AURKA have focused on activities of this kinase in mitosis, and elucidated the mechanisms by which AURKA activity is induced at the G2/M boundary through interactions with proteins such as TPX2 and NEDD9. These studies have informed the development of small molecule inhibitors of AURKA, of which a number are currently under preclinical and clinical assessment. While the first activities defined for AURKA were its control of centrosomal maturation and organization of the mitotic spindle, an increasing number of studies over the past decade have recognized a separate biological function of AURKA, in controlling disassembly of the primary cilium, a small organelle protruding from the cell surface that serves as a signaling platform. Importantly, these activities require activation of AURKA in early G1, and the mechanisms of activation are much less well defined than those in mitosis. A better understanding of the control of AURKA activity and the role of AURKA at cilia are both important in optimizing the efficacy and interpreting potential downstream consequences of AURKA inhibitors in the clinic. We here provide a current overview of proteins and mechanisms that have been defined as activating AURKA in G1, based on the study of ciliary disassembly.

Indexed as

MitosisSignal TransductionAnimalsAurora Kinase ACiliaEnzyme ActivationG1 PhaseHumansModels, BiologicalNeoplasmsAurora Kinase AAURKAciliaciliopathyhuman malignancyprotein–serine–threonine kinasessignal transduction

Identifiers

PMID28202658
PMCPMC5860652
OpenAlexW2588729701

What OpenQuestion holds

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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.