ArticlePloS one2014
Altering FAK-paxillin interactions reduces adhesion, migration and invasion processes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 107 citations in OpenAlex.
- Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026Review
- Submicron traction-force mapping reveals mitochondrial regulation of nanoscale force coordination during rigidity sensing under oxidative stress.Nano convergence · 2026Article
- Role of Focal Adhesion Kinase and NRF2 Pathways in Gastrointestinal Wound Healing.International journal of molecular sciences · 2026Review
- TRIM15 Mediates ubiquitination of Paxillin to facilitate the progression of ovarian cancer.Cancer cell international · 2026Article
- A role for PaxB in regulating blebbing: experimental insights and theoretical perspectives from Dictyostelium discoideum.BMC molecular and cell biology · 2026Article
- Review
- Establishing selectivity of FAK-paxillin PPI inhibitor using pulldown proteomics and a focal adhesion protein selectivity panel.Biochemistry and biophysics reports · 2026Article
- A phase separation hypothesis for the biological function of PrP: the role of multivalent interactions at the plasma membrane.Biochemical Society transactions · 2026Review
- A role for PaxB in regulating blebbing: experimental insights and theoretical perspectives fromResearch square · 2026Article
- Targeting the ST3 beta-galactoside alpha-2,3-sialyltransferase 1 (ST3Gal1) as a potential therapeutic strategy to overcome anti-VEGF resistance in endometrial cancer.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025Article
- Durotaxis is a driver and potential therapeutic target in lung fibrosis and metastatic pancreatic cancer.Nature cell biology · 2025Article
- Nf2-FAK signaling axis is critical for cranial bone ossification and regeneration.Nature communications · 2025Article
- Focal adhesion in the tumour metastasis: from molecular mechanisms to therapeutic targets.Biomarker research · 2025Review
- Structure-based discovery of hydrocarbon-stapled paxillin peptides that block FAK scaffolding in cancer.Nature communications · 2025Article
- Non-Receptor Tyrosine Kinases: Their Structure and Mechanistic Role in Tumor Progression and Resistance.Cancers · 2024Review
- Clinical Importance of Focal Adhesion Kinase (FAK)-Src and Paxillin Expression in Renal Cell Carcinoma.Cureus · 2024Article
- Effect of Crude Polysaccharides fromFoods (Basel, Switzerland) · 2024Article
- Oleanolic Acid Complexation with Cyclodextrins Improves Its Cell Bio-Availability and Biological Activities for Cell Migration.International journal of molecular sciences · 2023Article
- Surface-induced phase separation of reconstituted nascent integrin clusters on lipid membranes.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Role of Paxillin Aberrant Expression in Cancer and Its Potential as a Target for Cancer Therapy.International journal of molecular sciences · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal adhesion kinase (FAK) plays an important role in signal transduction pathways initiated at sites of integrin-mediated cell adhesion to the extracellular matrix. Thus, FAK is involved in many aspects of the metastatic process including adhesion, migration and invasion. Recently, several small molecule inhibitors which target FAK catalytic activity have been developed by pharmaceutical companies. The current study was aimed at addressing whether inhibiting FAK targeting to focal adhesions (FA) represents an efficient alternative strategy to inhibit FAK downstream pathways. Using a mutagenesis approach to alter the targeting domain of FAK, we constructed a FAK mutant that fails to bind paxillin. Inhibiting FAK-paxillin interactions led to a complete loss of FAK localization at FAs together with reduced phosphorylation of FAK and FAK targets such as paxillin and p130Cas. This in turn resulted in altered FA dynamics and inhibition of cell adhesion, migration and invasion. Moreover, the migration properties of cells expressing the FAK mutant were reduced as compared to FAK-/- cells. This was correlated with a decrease in both phospho-Src and phospho-p130Cas levels at FAs. We conclude that targeting FAK-paxillin interactions is an efficient strategy to reduce FAK signalling and thus may represent a target for the development of new FAK inhibitors.
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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.