ArticleMolecular biology of the cell1999
Focal adhesion targeting: the critical determinant of FAK regulation and substrate phosphorylation.
Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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
46 citing papers in PubMed, 124 citations in OpenAlex.
- Kinase condensates enrich ATP and trigger autophosphorylation.Cell reports · 2026Article
- The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling.Oncology research · 2026Article
- Structure-based discovery of hydrocarbon-stapled paxillin peptides that block FAK scaffolding in cancer.Nature communications · 2025Article
- Article
- Non-Receptor Tyrosine Kinases: Their Structure and Mechanistic Role in Tumor Progression and Resistance.Cancers · 2024Review
- Dietary Polyphenols Effects on Focal Adhesion Plaques and Metalloproteinases in Cancer Invasiveness.Biomedicines · 2024Review
- Oleanolic acid stimulation of cell migration involves a biphasic signaling mechanism.Scientific reports · 2022Article
- CK2β Is a Gatekeeper of Focal Adhesions Regulating Cell Spreading.Frontiers in molecular biosciences · 2022Article
- Regulation of the integrin αVβ3- actin filaments axis in early osteogenesis of human fibroblasts under cyclic tensile stress.Stem cell research & therapy · 2021Article
- FAK displacement from focal adhesions: a promising strategy to target processes implicated in cancer progression and metastasis.Cell communication and signaling : CCS · 2021Article
- Src Mediates Epigallocatechin-3-Molecules (Basel, Switzerland) · 2020Article
- Increased mitochondrial NADPH oxidase 4 (NOX4) expression in aging is a causative factor in aortic stiffening.Redox biology · 2019Article
- Review
- Inhibition of focal adhesion kinase overcomes resistance of mantle cell lymphoma to ibrutinib in the bone marrow microenvironment.Haematologica · 2018Article
- Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation.Scientific reports · 2017Article
- Design, synthesis, and biological evaluation of novel FAK scaffold inhibitors targeting the FAK-VEGFR3 protein-protein interaction.European journal of medicinal chemistry · 2014Article
- Mitsugumin 53 (MG53) ligase ubiquitinates focal adhesion kinase during skeletal myogenesis.The Journal of biological chemistry · 2014Article
- Altering FAK-paxillin interactions reduces adhesion, migration and invasion processes.PloS one · 2014Article
- Article
- A role for the protein tyrosine phosphatase CD45 in macrophage adhesion through the regulation of paxillin degradation.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The focal adhesion kinase (FAK) is discretely localized to focal adhesions via its C-terminal focal adhesion-targeting (FAT) sequence. FAK is regulated by integrin-dependent cell adhesion and can regulate tyrosine phosphorylation of downstream substrates, like paxillin. By the use of a mutational strategy, the regions of FAK that are required for cell adhesion-dependent regulation and for inducing tyrosine phosphorylation of paxillin were determined. The results show that the FAT sequence was the single region of FAK that was required for each function. Furthermore, the FAT sequence of FAK was replaced with a focal adhesion-targeting sequence from vinculin, and the resulting chimera exhibited cell adhesion-dependent tyrosine phosphorylation and could induce paxillin phosphorylation like wild-type FAK. These results suggest that subcellular localization is the major determinant of FAK function.
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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.