ArticleThe Biochemical journal2002
Characterization of an activated mutant of focal adhesion kinase: 'SuperFAK'.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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
33 citing papers in PubMed, 62 citations in OpenAlex.
- Focal adhesion kinase: A promising regulator of colitis-associated healing.World journal of gastroenterology · 2025Review
- Review
- Transcriptomic profiling in canines and humans reveals cancer specific gene modules and biological mechanisms common to both species.PLoS computational biology · 2021Article
- Molecular Regulation of the RhoGAP GRAF3 and Its Capacity to Limit Blood Pressure In Vivo.Cells · 2020Article
- FAK-Dependent Cell Motility and Cell Elongation.Cells · 2020Review
- Identification of a novel anoikis signalling pathway using the fungal virulence factor gliotoxin.Nature communications · 2018Article
- Focal Adhesion Kinase-mediated Phosphorylation of Beclin1 Protein Suppresses Cardiomyocyte Autophagy and Initiates Hypertrophic Growth.The Journal of biological chemistry · 2017Article
- Article
- Periostin induces intracellular cross-talk between kinases and hyaluronan in atrioventricular valvulogenesis.The Journal of biological chemistry · 2014Article
- Focal adhesion kinase antagonizes doxorubicin cardiotoxicity via p21(Cip1.).Journal of molecular and cellular cardiology · 2014Article
- Article
- 2-Hydroxyethyl methacrylate inhibits migration of dental pulp stem cells.Journal of endodontics · 2013Article
- Multiple steps to activate FAK's kinase domain: adaptation to confined environments?Biophysical journal · 2013Article
- Focal adhesion kinase modulates Cdc42 activity downstream of positive and negative axon guidance cues.Journal of cell science · 2012Article
- Targeted focal adhesion kinase activation in cardiomyocytes protects the heart from ischemia/reperfusion injury.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- β₁Integrin/FAK/cortactin signaling is essential for human head and neck cancer resistance to radiotherapy.The Journal of clinical investigation · 2012Article
- Prolactin-stimulated activation of ERK1/2 mitogen-activated protein kinases is controlled by PI3-kinase/Rac/PAK signaling pathway in breast cancer cells.Cellular signalling · 2011Article
- Article
- Focal adhesion kinase functions as an akt downstream target in migration of colorectal cancer cells.Translational oncology · 2009Article
- FRNK expression promotes smooth muscle cell maturation during vascular development and after vascular injury.Arteriosclerosis, thrombosis, and vascular biology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that plays an important role in normal cellular processes such as adhesion, spreading, migration, proliferation and survival. In addition, FAK is overexpressed in a variety of cancer cells and tumours and may play a role in the development of human cancer. As a prelude to modelling the role of aberrant FAK signalling in the initiation of cancer, the goal of the present study was to engineer point mutations in FAK that would enhance enzymic activity. A number of substitutions that were reported as activating mutations in other tyrosine kinases were introduced into FAK. Glutamic acid substitutions for two lysine residues in the activation loop of FAK, based upon the K650E (Lys(650-->)Glu) mutant of fibroblast-growth-factor receptor 3, were made to create 'SuperFAK'. Two brain-specific exons were engineered into avian FAK to create FAK6.7. SuperFAK and, to a lesser extent, FAK6.7, exhibited increased catalytic activity in vitro compared with wild-type FAK. The expression of SuperFAK and FAK6.7 in fibroblasts led to hyperphosphorylation of FAK substrates. Although the catalytic activity of SuperFAK and FAK6.7 was largely independent of cell adhesion, tyrosine phosphorylation of downstream substrates was adhesion-dependent. Further, since SuperFAK exhibited the same ability as wild-type FAK to recruit Src family kinases, tyrosine phosphorylation of substrates was likely due to direct phosphorylation by FAK. In addition to enhanced biochemical signalling, SuperFAK also increased the motility of epithelial cells. SuperFAK and FAK6.7 may be valuable molecular tools to investigate the potential role of aberrant FAK signalling in human disease.
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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.