ArticleThe Journal of cell biology2001
Marching at the front and dragging behind: differential alphaVbeta3-integrin turnover regulates focal adhesion behavior.
Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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Who cites it
161 citing papers in PubMed.
- Potential Role of the Urokinase-Type Plasminogen Activator Receptor-Integrin β3 Axis in Podocyte Adhesion Instability and Loss.Kidney international reports · 2026Article
- Organization and Dynamics of Focal Adhesions: Light Diffraction Analysis of Cellular Adhesion on Nanopatterned Surfaces.ACS applied materials & interfaces · 2026Article
- Talin-tensin3 interactions regulate fibrillar adhesion formation and tensin3 phase separation.The Journal of cell biology · 2026Article
- Substrate stiffness modulates phenotype-dependent fibroblast contractility and migration independent of TGF-Mechanobiology in medicine · 2025Article
- A tale of two distinct actin networks underlies the entire life cycle of focal adhesion.bioRxiv : the preprint server for biology · 2025Article
- Mechanical signaling regulates vascular smooth muscle cell adaptation in aging.Frontiers in physiology · 2025Article
- Epithelial cell-cell interactions in an overcrowded environment: jamming or live cell extrusion.Journal of biological engineering · 2024Review
- Extracellular lipidosomes containing lipid droplets and mitochondria are released during melanoma cell division.Cell communication and signaling : CCS · 2024Article
- Polarized focal adhesion kinase activity within a focal adhesion during cell migration.Nature chemical biology · 2023Article
- Smooth Muscle-Alpha Actin R149C Pathogenic Variant Downregulates Integrin Recruitment at Cell-Matrix Adhesions and Decreases Cellular Contractility.International journal of molecular sciences · 2023Article
- Mechanisms of Foreign Body Giant Cell Formation in Response to Implantable Biomaterials.Polymers · 2023Review
- Force tuning through regulation of clathrin-dependent integrin endocytosis.The Journal of cell biology · 2023Article
- Nox1-based NADPH oxidase regulates the Par protein complex activity to control cell polarization.Frontiers in cell and developmental biology · 2023Article
- Kinetic Changes of Ptdins (3,4,5) P3 within Fast and Slow Turnover Rates of Focal Adhesion.Reports of biochemistry & molecular biology · 2022Article
- Single-cell adhesivity distribution of glycocalyx digested cancer cells from high spatial resolution label-free biosensor measurements.Matrix biology plus · 2022Article
- Gut homeostasis, injury, and healing: New therapeutic targets.World journal of gastroenterology · 2022Review
- The restricted adhesion of bone marrow mesenchymal stem cells by stepped structures on surfaces of hydroxyapatite.RSC advances · 2022Article
- Paxillin: A Hub for Mechano-Transduction from the β3 Integrin-Talin-Kindlin Axis.Frontiers in cell and developmental biology · 2022Review
- Article
- Integrin intra-heterodimer affinity inversely correlates with integrin activatability.Cell reports · 2021Article
101 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Integrins are cell-substrate adhesion molecules that provide the essential link between the actin cytoskeleton and the extracellular matrix during cell migration. We have analyzed alphaVbeta3-integrin dynamics in migrating cells using a green fluorescent protein-tagged beta3-integrin chain. At the cell front, adhesion sites containing alphaVbeta3-integrin remain stationary, whereas at the rear of the cell they slide inward. The integrin fluorescence intensity within these different focal adhesions, and hence the relative integrin density, is directly related to their mobility. Integrin density is as much as threefold higher in sliding compared with stationary focal adhesions. High intracellular tension under the control of RhoA induced the formation of high-density contacts. Low-density adhesion sites were induced by Rac1 and low intracellular tension. Photobleaching experiments demonstrated a slow turnover of beta3-integrins in low-density contacts, which may account for their stationary nature. In contrast, the fast beta3-integrin turnover observed in high-density contacts suggests that their apparent sliding may be caused by a polarized renewal of focal contacts. Therefore, differential acto-myosin-dependent integrin turnover and focal adhesion densities may explain the mechanical and behavioral differences between cell adhesion sites formed at the front, and those that move in the retracting rear of migrating cells.
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