Evidence map›Paper›PMID 26111161›Full record

ArticlePloS one2015

Structure-Function Analysis of the Non-Muscle Myosin Light Chain Kinase (nmMLCK) Isoform by NMR Spectroscopy and Molecular Modeling: Influence of MYLK Variants.

Kui Shen, Benjamin Ramirez, Brandon Mapes, Grace R Shen, Vijay Gokhale, Mary E Brown, Bernard Santarsiero, Yoshitaka Ishii, Steven M Dudek, Ting Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Epigenetic contribution of the myosin light chain kinase gene to the risk for acute respiratory distress syndrome.Translational research : the journal of laboratory and clinical medicine · 2017
    Article
  9. Mechanical Stress and Single Nucleotide Variants Regulate Alternative Splicing of the MYLK Gene.American journal of respiratory cell and molecular biology · 2017
    Article
  10. 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

11 authors at 2 institutions in 1 country.

Kui ShenInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep, and Allergy, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Benjamin RamirezCenter for Structural Biology, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Brandon MapesInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep, and Allergy, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Grace R ShenInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep, and Allergy, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Vijay GokhaleCollege of Pharmacy and BIO5 Institute, University of Arizona, Tucson, Arizona, United States of America.
Mary E BrownInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep, and Allergy, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Bernard SantarsieroCenter for Structural Biology, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Yoshitaka IshiiCenter for Structural Biology, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Steven M DudekInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep, and Allergy, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Ting WangInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep, and Allergy, University of Illinois at Chicago, Chicago, Illinois, United States of America; Arizona Respiratory Center and Department of Medicine, University of Arizona, Tucson, Arizona, United States of America.
Joe G N GarciaInstitute for Personalized Respiratory Medicine, Section of Pulmonary, Critical Care, Sleep, and Allergy, University of Illinois at Chicago, Chicago, Illinois, United States of America; Arizona Respiratory Center and Department of Medicine, University of Arizona, Tucson, Arizona, United States of America.
University of Illinois Chicago · USUniversity of Arizona · US

Funding

Tissue Culture Biomechanical CoreP01HL058064 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAL, RATNESHWAR · 1998 to 2012
$27.8M
Structure-Function Analysis of nmMLCK in EC Barrier ResponsesP01HL126609 · NHLBI · UNIVERSITY OF FLORIDA · PI STEVEN M DUDEK · 2016 to 2026
$24.4M
Regulation of Asthmatic Inflammation by Non-Muscle MLCKR01HL091889 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GARCIA, JOE G. N., WANG, TING · 2008 to 2018
$3.2M
NHLBI NIH HHS HL058064NHLBI NIH HHS HL091889NHLBI NIH HHS P01 HL058064NHLBI NIH HHS P01 HL126609NHLBI NIH HHS R01 HL091889
6 · The paper itself

Abstract

The MYLK gene encodes the multifunctional enzyme, myosin light chain kinase (MLCK), involved in isoform-specific non-muscle and smooth muscle contraction and regulation of vascular permeability during inflammation. Three MYLK SNPs (P21H, S147P, V261A) alter the N-terminal amino acid sequence of the non-muscle isoform of MLCK (nmMLCK) and are highly associated with susceptibility to acute lung injury (ALI) and asthma, especially in individuals of African descent. To understand the functional effects of SNP associations, we examined the N-terminal segments of nmMLCK by 1H-15N heteronuclear single quantum correlation (HSQC) spectroscopy, a 2-D NMR technique, and by in silico molecular modeling. Both NMR analysis and molecular modeling indicated SNP localization to loops that connect the immunoglobulin-like domains of nmMLCK, consistent with minimal structural changes evoked by these SNPs. Molecular modeling analysis identified protein-protein interaction motifs adversely affected by these MYLK SNPs including binding by the scaffold protein 14-3-3, results confirmed by immunoprecipitation and western blot studies. These structure-function studies suggest novel mechanisms for nmMLCK regulation, which may confirm MYLK as a candidate gene in inflammatory lung disease and advance knowledge of the genetic underpinning of lung-related health disparities.

Indexed as

Structure-Activity RelationshipBlack PeopleHumansLung DiseasesMagnetic Resonance SpectroscopyModels, MolecularMyosin-Light-Chain KinaseNuclear Magnetic Resonance, BiomolecularPhosphorylationPolymorphism, Single NucleotideProtein IsoformsMyosin-Light-Chain Kinasenon-muscle myosin light-chain kinase, humanProtein Isoforms

Identifiers

PMID26111161
PMCPMC4482139
OpenAlexW1148358250

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.