ArticleThe Journal of biological chemistry2013
Glia maturation factor (GMF) interacts with Arp2/3 complex in a nucleotide state-dependent manner.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Inorganic phosphate rapidly switches the stability of Arp2/3-induced actin branches.The Journal of cell biology · 2026Article
- Mechanism of Arp2/3 complex branch disassembly by human Coro7.Nature communications · 2025Article
- The role of actin cytoskeleton component Arp2/3 in inflammatory response.Frontiers in cell and developmental biology · 2025Review
- Cryo-EM structures reveal how phosphate release from Arp3 weakens actin filament branches formed by Arp2/3 complex.Nature communications · 2024Article
- Direct observation of cortactin protecting Arp2/3-actin filament branch junctions from GMF-mediated destabilization.European journal of cell biology · 2024Article
- The stabilization of Arp2/3 complex generated actin filaments.Biochemical Society transactions · 2024Review
- Mechanisms of actin disassembly and turnover.The Journal of cell biology · 2023Review
- Glia maturation factor-γ is required for initiation and maintenance of hematopoietic stem and progenitor cells.Stem cell research & therapy · 2023Article
- Biochemical and mechanical regulation of actin dynamics.Nature reviews. Molecular cell biology · 2022Review
- IRSp53 promotes postsynaptic density formation and actin filament bundling.The Journal of cell biology · 2022Article
- Nucleation, stabilization, and disassembly of branched actin networks.Trends in cell biology · 2022Review
- GMFG (glia maturation factor gamma) inhibits lung cancer growth by activating p53 signaling pathway.Bioengineered · 2022Article
- Deletion of gmfA induces keratocyte-like migration in Dictyostelium.FEBS open bio · 2022Article
- 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
- Force and phosphate release from Arp2/3 complex promote dissociation of actin filament branches.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Cellular and pathophysiological consequences of Arp2/3 complex inhibition: role of inhibitory proteins and pharmacological compounds.Cellular and molecular life sciences : CMLS · 2019Review
- GMF as an Actin Network Remodeling Factor.Trends in cell biology · 2018Review
- Glia maturation factor-β: a potential therapeutic target in neurodegeneration and neuroinflammation.Neuropsychiatric disease and treatment · 2018Review
- Function and regulation of the Arp2/3 complex during cell migration in diverse environments.Current opinion in cell biology · 2016Review
- Role and structural mechanism of WASP-triggered conformational changes in branched actin filament nucleation by Arp2/3 complex.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glia maturation factor (GMF) is a member of the actin-depolymerizing factor (ADF)/cofilin family. ADF/cofilin promotes disassembly of aged actin filaments, whereas GMF interacts specifically with Arp2/3 complex at branch junctions and promotes debranching. A distinguishing feature of ADF/cofilin is that it binds tighter to ADP-bound than to ATP-bound monomeric or filamentous actin. The interaction is also regulated by phosphorylation at Ser-3 of mammalian cofilin, which inhibits binding to actin. However, it is unknown whether these two factors play a role in the interaction of GMF with Arp2/3 complex. Here we show using isothermal titration calorimetry that mammalian GMF has very low affinity for ATP-bound Arp2/3 complex but binds ADP-bound Arp2/3 complex with 0.7 μM affinity. The phosphomimetic mutation S2E in GMF inhibits this interaction. GMF does not bind monomeric ATP- or ADP-actin, confirming its specificity for Arp2/3 complex. We further show that mammalian Arp2/3 complex nucleation activated by the WCA region of the nucleation-promoting factor N-WASP is not affected by GMF, whereas nucleation activated by the WCA region of WAVE2 is slightly inhibited at high GMF concentrations. Together, the results suggest that GMF functions by a mechanism similar to that of other ADF/cofilin family members, displaying a preference for ADP-Arp2/3 complex and undergoing inhibition by phosphorylation of a serine residue near the N terminus. Arp2/3 complex nucleation occurs in the ATP state, and nucleotide hydrolysis promotes debranching, suggesting that the higher affinity of GMF for ADP-Arp2/3 complex plays a physiological role by promoting debranching of aged branch junctions without interfering with Arp2/3 complex nucleation.
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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.