Evidence map›Paper›PMID 23226601›Full record

ReviewOpen biology2012

On the molecular mechanisms of mitotic kinase activation.

Richard Bayliss, Andrew Fry, Tamanna Haq, Sharon Yeoh

Open access · goldAbstract readReview
In one paragraph

Review in Open biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 117 citations in OpenAlex.

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2 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 1 institution in 1 country.

Richard BaylissDepartment of Biochemistry, Henry Wellcome Laboratories for Structural Biology, University of Leicester, Lancaster Road, Leicester LE1 9HN, UK. richard.bayliss@le.ac.uk
Andrew Fry
Tamanna Haq
Sharon Yeoh
University of Leicester · GB

Funding

Cancer Research UK 12772Cancer Research UK C24461/A12772Cancer Research UK C24461/A13231Wellcome Trust
6 · The paper itself

Abstract

During mitosis, human cells exhibit a peak of protein phosphorylation that alters the behaviour of a significant proportion of proteins, driving a dramatic transformation in the cell's shape, intracellular structures and biochemistry. These mitotic phosphorylation events are catalysed by several families of protein kinases, including Auroras, Cdks, Plks, Neks, Bubs, Haspin and Mps1/TTK. The catalytic activities of these kinases are activated by phosphorylation and through protein-protein interactions. In this review, we summarize the current state of knowledge of the structural basis of mitotic kinase activation mechanisms. This review aims to provide a clear and comprehensive primer on these mechanisms to a broad community of researchers, bringing together the common themes, and highlighting specific differences. Along the way, we have uncovered some features of these proteins that have previously gone unreported, and identified unexplored questions for future work. The dysregulation of mitotic kinases is associated with proliferative disorders such as cancer, and structural biology will continue to play a critical role in the development of chemical probes used to interrogate disease biology and applied to the treatment of patients.

Indexed as

AnimalsCell Cycle ProteinsEnzyme ActivationFeedback, PhysiologicalGene Expression RegulationHumansKineticsMitosisModels, MolecularNeoplasmsPhosphorylationProtein KinasesSpindle ApparatusXenopus laevisZebrafishCell Cycle ProteinsProtein Kinasesmitosisprotein kinasesprotein structuresregulation

Identifiers

PMID23226601
PMCPMC3513839
OpenAlexW2011290290

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.