ArticleEuropean journal of human genetics : EJHG2015
A MYLK variant regulates asthmatic inflammation via alterations in mRNA secondary structure.
Article in European journal of human genetics : EJHG, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Systems-level transcriptomic analysis reveals synapse-related gene dysregulation in peripheral leukocytes of MDD patients.Scientific reports · 2026Pooled it
- Review
- A Razor's Edge: Vascular Responses to Acute Inflammatory Lung Injury/Acute Respiratory Distress Syndrome.Annual review of physiology · 2024Review
- Non-Muscle MLCK Contributes to Endothelial Cell Hyper-Proliferation through the ERK Pathway as a Mechanism for Vascular Remodeling in Pulmonary Hypertension.International journal of molecular sciences · 2022Article
- Critical role for the lung endothelial nonmuscle myosin light-chain kinase isoform in the severity of inflammatory murine lung injury.Pulmonary circulation · 2022Article
- Postnatal development alters functional compartmentalization of myosin light chain kinase in ovine carotid arteries.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Hypoxic modulation of fetal vascular MLCK abundance, localization, and function.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- RPA1 binding to NRF2 switches ARE-dependent transcriptional activation to ARE-NRE-dependent repression.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The myosin light-chain kinase MLCK-1 relocalizes during Caenorhabditis elegans ovulation to promote actomyosin bundle assembly and drive contraction.Molecular biology of the cell · 2018Article
- The roles of RNA processing in translating genotype to phenotype.Nature reviews. Molecular cell biology · 2017Review
- 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 · 2017Article
- Mechanical Stress and Single Nucleotide Variants Regulate Alternative Splicing of the MYLK Gene.American journal of respiratory cell and molecular biology · 2017Article
- Myosin Light Chain Kinase: A Potential Target for Treatment of Inflammatory Diseases.Frontiers in pharmacology · 2017Review
- Nonmuscle myosin light chain kinase activity modulates radiation-induced lung injury.Pulmonary circulation · 2016Article
- Sp1-mediated nonmuscle myosin light chain kinase expression and enhanced activity in vascular endothelial growth factor-induced vascular permeability.Pulmonary circulation · 2015Article
- Functional and Structural Consequence of Rare Exonic Single Nucleotide Polymorphisms: One Story, Two Tales.Genome biology and evolution · 2015Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Myosin light-chain kinase (MYLK) is a gene known to be significantly associated with severe asthma in African Americans. Here we further examine the molecular function of a single-nucleotide polymorphism (SNP), located in the non-muscle myosin light-chain kinase isoform (nmMLCK), in asthma susceptibility and pathobiology. We identified nmMLCK variant (reference SNP: rs9840993, NM_053025: 721C>T, c.439C>T) with a distinct mRNA secondary structure from the other variants. The nmMLCK variant (721C) secondary structure exhibits increased stability with an elongated half-life in the human endothelial cell, and greater efficiency in protein translation initiation owing to an increased accessibility to translation start site. Finally, nmMLCK expression of 721C- and 721T-containing MYLK transgenes were compared in nmMLCK(-/-) mice and confirmed deleterious effects of nmMLCK expression on asthmatic indices and implicated the augmented influence of MYLK 721C>T (c.439C>T) SNP on asthma severity. The confirmation of the novel mechanism of the regulation of asthmatic inflammation by a MYLK advances knowledge of the genetic basis for asthma disparities, and further suggests the potential of nmMLCK as a therapeutic target. Our study suggests that in addition to altering protein structure and function, non-synonymous SNPs may also lead to phenotypic disparity by altering protein expression.
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Registered trials
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.