ArticleAmerican journal of respiratory cell and molecular biology2014
Glia maturation factor-γ phosphorylation at Tyr-104 regulates actin dynamics and contraction in human airway smooth muscle.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- TET1 Regulates Nestin Expression and Human Airway Smooth Muscle Proliferation.American journal of respiratory cell and molecular biology · 2024Article
- Membrane adhesion junctions regulate airway smooth muscle phenotype and function.Physiological reviews · 2023Review
- The intermediate filament protein nestin serves as a molecular hub for smooth muscle cytoskeletal signaling.Respiratory research · 2023Article
- Demystifying Bitter Taste Receptor Relaxation of Airway Smooth Muscle.American journal of respiratory cell and molecular biology · 2023Article
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- Abi1 mediates airway smooth muscle cell proliferation and airway remodeling via Jak2/STAT3 signaling.iScience · 2022Article
- Airway smooth muscle and airway hyperresponsiveness in asthma: mechanisms of airway smooth muscle dysfunction.Minerva medica · 2022Article
- Plk1 Regulates Caspase-9 Phosphorylation at Ser-196 and Apoptosis of Human Airway Smooth Muscle Cells.American journal of respiratory cell and molecular biology · 2022Article
- Acetylation of Abelson interactor 1 at K416 regulates actin cytoskeleton and smooth muscle contraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Article
- The Actin-Disassembly Protein Glia Maturation Factor γ Enhances Actin Remodeling and B Cell Antigen Receptor Signaling at the Immune Synapse.Frontiers in cell and developmental biology · 2021Article
- Distinctive roles of Abi1 in regulating actin-associated proteins during human smooth muscle cell migration.Scientific reports · 2020Article
- Ste20-like Kinase-mediated Control of Actin Polymerization Is a New Mechanism for Thin Filament-associated Regulation of Airway Smooth Muscle Contraction.American journal of respiratory cell and molecular biology · 2020Article
- Cellular and pathophysiological consequences of Arp2/3 complex inhibition: role of inhibitory proteins and pharmacological compounds.Cellular and molecular life sciences : CMLS · 2019Review
- Orchestrating Airway Smooth Muscle Cell Migration: GMFγ Phosphorylation Is the Key.American journal of respiratory cell and molecular biology · 2019Article
- Phosphorylation of GMFγ by c-Abl Coordinates Lamellipodial and Focal Adhesion Dynamics to Regulate Airway Smooth Muscle Cell Migration.American journal of respiratory cell and molecular biology · 2019Article
- Plk1 Mediates Paxillin Phosphorylation (Ser-272), Centrosome Maturation, and Airway Smooth Muscle Layer Thickening in Allergic Asthma.Scientific reports · 2019Article
- Glia maturation factor-γ regulates murine macrophage iron metabolism and M2 polarization through mitochondrial ROS.Blood advances · 2019Article
- Specific protein 1, c-Abl and ERK1/2 form a regulatory loop.Journal of cell science · 2019Article
- GMF as an Actin Network Remodeling Factor.Trends in cell biology · 2018Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Actin dynamics plays an essential role in regulating airway smooth muscle contraction. The mechanisms that regulate actin dynamics in smooth muscle are not completely understood. Glia maturation factor (GMF) is a protein that has been reported to inhibit actin nucleation and to induce actin network debranching in vitro. The role of GMF in human smooth muscle cells and tissues has not been investigated. In this study, knockdown of GMF-γ by RNA interference enhanced actin polymerization and contraction in human airway smooth muscle (HASM) cells and tissues without affecting myosin phosphorylation (another important biochemical change during contractile activation). Activation of HASM cells and tissues with acetylcholine induced dissociation of GMF-γ from Arp2 of the Arp2/3 complex. Acetylcholine stimulation also increased GMF-γ phosphorylation at Tyr-104. GMF-γ phosphorylation at this residue was mediated by c-Abl tyrosine kinase. The GMF-γ mutant Y104F (phenylalanine substitution at Tyr-104) had higher association with Arp2 in HASM cells upon contractile activation. Furthermore, expression of mutant Y104F GMF-γ attenuated actin polymerization and contraction in smooth muscle. Thus, we propose a novel mechanism for the regulation of actin dynamics and smooth muscle contraction. In unstimulated smooth muscle, GMF-γ binds to the Arp2/3 complex, which induces actin disassembly and retains lower levels of F-actin. Upon contractile stimulation, phosphorylation at Tyr-104 mediated by c-Abl tyrosine kinase leads to the dissociation of GMF-γ from Arp2/3, by which GMF-γ no longer induces actin disassembly. Reduced actin disassembly renders F-actin in higher level, which facilitates smooth muscle contraction.
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