Evidence map›Paper›PMID 26925779›Full record

ArticlePLoS genetics2016

Hydrophobic Core Variations Provide a Structural Framework for Tyrosine Kinase Evolution and Functional Specialization.

Smita Mohanty, Krishnadev Oruganty, Annie Kwon, Dominic P Byrne, Samantha Ferries, Zheng Ruan, Laura E Hanold, Samiksha Katiyar, Eileen J Kennedy, Patrick A Eyers and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

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  14. Lipid-targeting pleckstrin homology domain turns its autoinhibitory face toward the TEC kinases.Proceedings of the National Academy of Sciences of the United States of America · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Smita MohantyDepartment of Biochemistry & Molecular Biology, University of Georgia, Athens, Georgia, United States of America.
Krishnadev OrugantyDepartment of Biochemistry & Molecular Biology, University of Georgia, Athens, Georgia, United States of America.
Annie KwonInstitute of Bioinformatics, University of Georgia, Athens, Georgia, United States of America.
Dominic P ByrneDepartment of Biochemistry, Institute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom.
Samantha FerriesDepartment of Biochemistry, Institute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom.
Zheng RuanInstitute of Bioinformatics, University of Georgia, Athens, Georgia, United States of America.
Laura E HanoldDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
Samiksha KatiyarDepartment of Biochemistry & Molecular Biology, University of Georgia, Athens, Georgia, United States of America.
Eileen J KennedyDepartment of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia, United States of America.
Patrick A EyersDepartment of Biochemistry, Institute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom.
Natarajan KannanDepartment of Biochemistry & Molecular Biology, University of Georgia, Athens, Georgia, United States of America.
University of Georgia · USUniversity of Liverpool · GB

Funding

Functional Annotation of Natural and Disease Variants in Tryosine KinasesR01GM114409 · NIGMS · UNIVERSITY OF GEORGIA · PI KANNAN, NATARAJAN · 2015 to 2020
$1.6M
Targeted Inhibition of EGFR DimerizationR03CA188439 · NCI · UNIVERSITY OF GEORGIA · PI KENNEDY, EILEEN J · 2015 to 2016
$150k
NCI NIH HHS R03 CA188439NIGMS NIH HHS GM114409-01NIGMS NIH HHS R01 GM114409
6 · The paper itself

Abstract

Protein tyrosine kinases (PTKs) are a group of closely related enzymes that have evolutionarily diverged from serine/threonine kinases (STKs) to regulate pathways associated with multi-cellularity. Evolutionary divergence of PTKs from STKs has occurred through accumulation of mutations in the active site as well as in the commonly conserved hydrophobic core. While the functional significance of active site variations is well understood, relatively little is known about how hydrophobic core variations contribute to PTK evolutionary divergence. Here, using a combination of statistical sequence comparisons, molecular dynamics simulations, mutational analysis and in vitro thermostability and kinase assays, we investigate the structural and functional significance of key PTK-specific variations in the kinase core. We find that the nature of residues and interactions in the hydrophobic core of PTKs is strikingly different from other protein kinases, and PTK-specific variations in the core contribute to functional divergence by altering the stability and dynamics of the kinase domain. In particular, a functionally critical STK-conserved histidine that stabilizes the regulatory spine in STKs is selectively mutated to an alanine, serine or glutamate in PTKs, and this loss-of-function mutation is accommodated, in part, through compensatory PTK-specific interactions in the core. In particular, a PTK-conserved phenylalanine in the I-helix appears to structurally and functionally compensate for the loss of STK-histidine by interacting with the regulatory spine, which has far-reaching effects on enzyme activity, inhibitor sensing, and stability. We propose that hydrophobic core variations provide a selective advantage during PTK evolution by increasing the conformational flexibility, and therefore the allosteric potential of the kinase domain. Our studies also suggest that Tyrosine Kinase Like kinases such as RAF are intermediates in PTK evolutionary divergence inasmuch as they share features of both PTKs and STKs in the core. Finally, our studies provide an evolutionary framework for identifying and characterizing disease and drug resistance mutations in the kinase core.

Indexed as

Evolution, MolecularAmino Acid SequenceAurora Kinase ACatalytic DomainConserved SequenceHydrophobic and Hydrophilic InteractionsMolecular Dynamics SimulationMolecular Sequence DataMutationProtein Kinase InhibitorsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesReceptor, EphA3Receptor Protein-Tyrosine KinasesStructure-Activity RelationshipAurora Kinase AEPHA3 protein, humanProtein Kinase InhibitorsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesReceptor, EphA3Receptor Protein-Tyrosine Kinases

Identifiers

PMID26925779
PMCPMC4771162
OpenAlexW2289184477

What OpenQuestion holds

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LicenceCC BY
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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.