ArticleMolecular biology of the cell2011
FAK phosphorylation at Tyr-925 regulates cross-talk between focal adhesion turnover and cell protrusion.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.
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Who cites it
87 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
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- Phospho-regulated tethering of focal adhesion kinase to vinculin links force transduction to focal adhesion signaling.Cell communication and signaling : CCS · 2025Article
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- Oleanolic Acid Complexation with Cyclodextrins Improves Its Cell Bio-Availability and Biological Activities for Cell Migration.International journal of molecular sciences · 2023Article
- The Neurod1/4-Ntrk3-Src pathway regulates gonadotrope cell adhesion and motility.Cell death discovery · 2023Article
- On the Value of In Vitro Cell Systems for Mechanobiology from the Perspective of Yes-Associated Protein/Transcriptional Co-Activator with a PDZ-Binding Motif and Focal Adhesion Kinase and Their Involvement in Wound Healing, Cancer, Aging, and Senescence.International journal of molecular sciences · 2023Review
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- Protein dynamics at invadopodia control invasion-migration transitions in melanoma cells.Cell death & disease · 2023Article
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- TMEM123 a key player in immune surveillance of colorectal cancer.Frontiers in immunology · 2023Article
- Complexity of progranulin mechanisms of action in mesothelioma.Journal of experimental & clinical cancer research : CR · 2022Article
- ZINC40099027 promotes monolayer circular defect closure by a novel pathway involving cytosolic activation of focal adhesion kinase and downstream paxillin and ERK1/2.Cell and tissue research · 2022Article
- Oleanolic acid stimulation of cell migration involves a biphasic signaling mechanism.Scientific reports · 2022Article
27 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell migration is a highly complex process that requires the coordinated formation of membrane protrusion and focal adhesions (FAs). Focal adhesion kinase (FAK), a major signaling component of FAs, is involved in the disassembly process of FAs through phosphorylation and dephosphorylation of its tyrosine residues, but the role of such phosphorylations in nascent FA formation and turnover near the cell front and in cell protrusion is less well understood. In the present study, we demonstrate that, depending on the phosphorylation status of Tyr-925 residue, FAK modulates cell migration via two specific mechanisms. FAK⁻/⁻ mouse embryonic fibroblasts (MEFs) expressing nonphosphorylatable Y925F-FAK show increased interactions between FAK and unphosphorylated paxillin, which lead to FA stabilization and thus decreased FA turnover and reduced cell migration. Conversely, MEFs expressing phosphomimetic Y925E-FAK display unchanged FA disassembly rates, show increase in phosphorylated paxillin in FAs, and exhibit increased formation of nascent FAs at the cell leading edges. Moreover, Y925E-FAK cells present enhanced cell protrusion together with activation of the p130(CAS)/Dock180/Rac1 signaling pathway. Together, our results demonstrate that phosphorylation of FAK at Tyr-925 is required for FAK-mediated cell migration and cell protrusion.
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