Evidence map›Paper›PMID 36266340›Full record

ArticleNature communications2022

NIMA-related kinase 9 regulates the phosphorylation of the essential myosin light chain in the heart.

Marion Müller, Rose Eghbalian, Jes-Niels Boeckel, Karen S Frese, Jan Haas, Elham Kayvanpour, Farbod Sedaghat-Hamedani, Maximilian K Lackner, Oguz F Tugrul, Thomas Ruppert and 16 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. The emerging role of Never-in-Mitosis A - Related Kinases in the endothelium.The international journal of biochemistry & cell biology · 2024
    Review
  7. Review
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

26 authors at 4 institutions in 2 countries.

Marion MüllerKardiogenetikzentrum Heidelberg, University Hospital of Heidelberg, Heidelberg, Germany.ORCID 0000-0002-8519-0661
Rose EghbalianKardiogenetikzentrum Heidelberg, University Hospital of Heidelberg, Heidelberg, Germany.
Jes-Niels BoeckelClinic and Polyclinic for Cardiology, University of Leipzig, Leipzig, Germany.ORCID 0000-0002-7438-3089
Karen S FreseDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.ORCID 0000-0003-1822-8559
Jan HaasDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Elham KayvanpourDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Farbod Sedaghat-HamedaniDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.ORCID 0000-0002-3266-0527
Maximilian K LacknerDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Oguz F TugrulDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Thomas RuppertCFMP, Core Facility for Mass Spectrometry & Proteomics at ZMBH, Heidelberg University, Heidelberg, Germany.
Rewati TappuDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Diana Martins BordaloDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Jasmin M KneuerClinic and Polyclinic for Cardiology, University of Leipzig, Leipzig, Germany.ORCID 0000-0003-0273-3614
Annika PiekarekDepartment of Medicine III, University of Heidelberg, Heidelberg, Germany.ORCID 0000-0002-2948-9642
Sabine HerchDepartment of Medicine III, University of Heidelberg, Heidelberg, Germany.
Sarah SchudyDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Andreas KellerClinical Bioinformatics, Saarland University, Saarbrücken, Germany.ORCID 0000-0002-5361-0895
Nadja GrammesClinical Bioinformatics, Saarland University, Saarbrücken, Germany.
Cornelius BischofClinic for General and Interventional Cardiology/ Angiology, Herz- und Diabeteszentrum NRW, University Hospital of the Ruhr-Universität Bochum, Bad Oeynhausen, Germany.ORCID 0000-0001-8496-2853
Anna KlinkeClinic for General and Interventional Cardiology/ Angiology, Herz- und Diabeteszentrum NRW, University Hospital of the Ruhr-Universität Bochum, Bad Oeynhausen, Germany.
Margarida Cardoso-MoreiraZMBH, Center for Molecular Biology, Heidelberg University, Heidelberg, Germany.ORCID 0000-0001-6639-3597
Henrik KaessmannZMBH, Center for Molecular Biology, Heidelberg University, Heidelberg, Germany.ORCID 0000-0001-7563-839X
Hugo A KatusDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Norbert FreyDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.
Lars M SteinmetzDZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Berlin, Germany.ORCID 0000-0002-3962-2865
Benjamin MederKardiogenetikzentrum Heidelberg, University Hospital of Heidelberg, Heidelberg, Germany. benjamin.meder@med.uni-heidelberg.de.ORCID 0000-0003-0741-2633
Heidelberg University · DEHeart and Diabetes Center North Rhine-Westphalia · DESaarland University · DEGerman Centre for Cardiovascular Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To adapt to changing hemodynamic demands, regulatory mechanisms modulate actin-myosin-kinetics by calcium-dependent and -independent mechanisms. We investigate the posttranslational modification of human essential myosin light chain (ELC) and identify NIMA-related kinase 9 (NEK9) to interact with ELC. NEK9 is highly expressed in the heart and the interaction with ELC is calcium-dependent. Silencing of NEK9 results in blunting of calcium-dependent ELC-phosphorylation. CRISPR/Cas9-mediated disruption of NEK9 leads to cardiomyopathy in zebrafish. Binding to ELC is mediated via the protein kinase domain of NEK9. A causal relationship between NEK9 activity and ELC-phosphorylation is demonstrated by genetic sensitizing in-vivo. Finally, we observe significantly upregulated ELC-phosphorylation in dilated cardiomyopathy patients and provide a unique map of human ELC-phosphorylation-sites. In summary, NEK9-mediated ELC-phosphorylation is a calcium-dependent regulatory system mediating cardiac contraction and inotropy.

Indexed as

ActinsMyosin Light ChainsAnimalsCalciumHumansNIMA-Related KinasesPhosphorylationProtein KinasesZebrafishActinsCalciumMyosin Light ChainsNEK9 protein, humanNIMA-Related KinasesProtein Kinases

Identifiers

PMID36266340
PMCPMC9585074
OpenAlexW4306862051

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.