ArticleMolecular and cellular biology2007
Extracellular signal-regulated kinase/mitogen-activated protein kinase regulates actin organization and cell motility by phosphorylating the actin cross-linking protein EPLIN.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 80 citations in OpenAlex.
- CDK1-mediated phosphorylation of EPLIN is crucial for mitotic spindle positioning.Communications biology · 2026Article
- Bisphosphate nucleotidase 1 promotes progression and docetaxel resistance in triple-negative breast cancer via STUB1-mediated destabilization of LIMA1.Cell death & disease · 2026Article
- An antagonistic role of clock genes and lima1 in kidney regeneration.Communications biology · 2025Article
- EPLIN, a prospective oncogenic molecule with contribution to growth, migration and drug resistance in pancreatic cancer.Scientific reports · 2024Article
- The concerted action of SEPT9 and EPLIN modulates the adhesion and migration of human fibroblasts.Life science alliance · 2024Article
- Exploring the Enigma: The Role of the Epithelial Protein Lost in Neoplasm in Normal Physiology and Cancer Pathogenesis.International journal of molecular sciences · 2024Review
- Role of Mitogen-Activated Protein (MAP) Kinase Pathways in Metabolic Diseases.Genome integrity · 2024Review
- Multiomics approach to profiling Sertoli cell maturation during development of the spermatogonial stem cell niche.Molecular human reproduction · 2023Article
- Characterization of LIMA1 and its emerging roles and potential therapeutic prospects in cancers.Frontiers in oncology · 2023Review
- BI-847325, a selective dual MEK and Aurora kinases inhibitor, reduces aggressive behavior of anaplastic thyroid carcinoma on an in vitro three-dimensional culture.Cancer cell international · 2022Article
- Protective effects of the postbiotic deriving from cow's milk fermentation with L. paracasei CBA L74 against Rotavirus infection in human enterocytes.Scientific reports · 2022Article
- Lima1 mediates the pluripotency control of membrane dynamics and cellular metabolism.Nature communications · 2022Article
- Epithelial Protein Lost in Neoplasm, EPLIN, the Cellular and Molecular Prospects in Cancers.Biomolecules · 2021Review
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- Identification of hub genes and pathways in cholangiocarcinoma by coexpression analysis.Cancer biomarkers : section A of Disease markers · 2020Article
- TRPC6 Binds to and Activates Calpain, Independent of Its Channel Activity, and Regulates Podocyte Cytoskeleton, Cell Adhesion, and Motility.Journal of the American Society of Nephrology : JASN · 2019Article
- Inhibition of ERK1/2 Restores GSK3β Activity and Protein Synthesis Levels in a Model of Tuberous Sclerosis.Scientific reports · 2017Article
- Epithelial protein lost in neoplasm (EPLIN): Beyond a tumor suppressor.Genes & diseases · 2017Review
- Human phosphatase CDC14A regulates actin organization through dephosphorylation of epithelial protein lost in neoplasm.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular signal-regulated kinase (ERK) is important for various cellular processes, including cell migration. However, the detailed molecular mechanism by which ERK promotes cell motility remains elusive. Here we characterize epithelial protein lost in neoplasm (EPLIN), an F-actin cross-linking protein, as a novel substrate for ERK. ERK phosphorylates Ser360, Ser602, and Ser692 on EPLIN in vitro and in intact cells. Phosphorylation of the C-terminal region of EPLIN reduces its affinity for actin filaments. EPLIN colocalizes with actin stress fibers in quiescent cells, and stimulation with platelet-derived growth factor (PDGF) induces stress fiber disassembly and relocalization of EPLIN to peripheral and dorsal ruffles, wherein phosphorylation of Ser360 and Ser602 is observed. Phosphorylation of these two residues is also evident during wound healing at the leading edge of migrating cells. Moreover, expression of a non-ERK-phosphorylatable mutant, but not wild-type EPLIN, prevents PDGF-induced stress fiber disassembly and membrane ruffling and also inhibits wound healing and PDGF-induced cell migration. We propose that ERK-mediated phosphorylation of EPLIN contributes to actin filament reorganization and enhanced cell motility.
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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.