ArticleeLife2023
ERK3/MAPK6 dictates CDC42/RAC1 activity and ARP2/3-dependent actin polymerization.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- MTSS1-dependent ubiquitin modifications mediated by FBXO44 remodel the actin cytoskeleton to promote gastric cancer progression.Molecular cancer · 2026Article
- Membrane Curvature and Cancer: Mechanisms, Implications, and Therapeutic Perspectives.Cancers · 2026Review
- Low YTHDC1 Expression Upregulates FSCN1 to Promote Nuclear F-Actin Formation and Facilitate Double-strand DNA Breaks Repair in TMZ-Resistant Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell transcriptomics reveals stepwise transformation of epithelial cells into Non-Professional Phagocytes.PLoS genetics · 2025Article
- Chaperone-mediated autophagy sustains muscle stem cell regenerative functions but declines with age.Nature metabolism · 2025Article
- Intracellular pH regulates ubiquitin-mediated degradation of the MAP kinase ERK3.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Orchestrating movement: the role of Caveolin-1 in migration and metastasis.Molecular cancer · 2025Review
- Akt-phosphorylated UFL1 UFMylates ArpC4 to promote metastasis.Nature structural & molecular biology · 2025Article
- Identification of characteristic genes ofanddeficiency constitutions: an integrated analysis based on bioinformatics and machine learning.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Atypical MAPKs in cancer.The FEBS journal · 2025Review
- Article
- The role of actin cytoskeleton component Arp2/3 in inflammatory response.Frontiers in cell and developmental biology · 2025Review
- ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity.Frontiers in oncology · 2025Article
- Clearing Amyloid-Beta by Astrocytes: The Role of Rho GTPases Signaling Pathways as Potential Therapeutic Targets.Brain sciences · 2024Review
- Rac1 inhibition regenerates wounds in mouse fetuses via altered actin dynamics.Scientific reports · 2024Article
- Identification of metabolic biomarkers in idiopathic pulmonary arterial hypertension using targeted metabolomics and bioinformatics analysis.Scientific reports · 2024Article
- Proangiogenic effect and underlying mechanism of holmium oxide nanoparticles: a new biomaterial for tissue engineering.Journal of nanobiotechnology · 2024Article
- Review
- Aggravated Ulcerative Colitis via circNlgn-Mediated Suppression of Nuclear Actin Polymerization.Research (Washington, D.C.) · 2024Article
- Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The actin cytoskeleton is tightly controlled by RhoGTPases, actin binding-proteins and nucleation-promoting factors to perform fundamental cellular functions. We have previously shown that ERK3, an atypical MAPK, controls IL-8 production and chemotaxis (Bogueka et al., 2020). Here, we show in human cells that ERK3 directly acts as a guanine nucleotide exchange factor for CDC42 and phosphorylates the ARP3 subunit of the ARP2/3 complex at S418 to promote filopodia formation and actin polymerization, respectively. Consistently, depletion of ERK3 prevented both basal and EGF-dependent RAC1 and CDC42 activation, maintenance of F-actin content, filopodia formation, and epithelial cell migration. Further, ERK3 protein bound directly to the purified ARP2/3 complex and augmented polymerization of actin in vitro. ERK3 kinase activity was required for the formation of actin-rich protrusions in mammalian cells. These findings unveil a fundamentally unique pathway employed by cells to control actin-dependent cellular functions.
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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.