Int J Biol Sci 2015; 11(4):404-410. doi:10.7150/ijbs.10273 This issue

Short Research Communication

Identification of Novel Focal Adhesion Kinase Substrates: Role for FAK in NFκB Signaling

Sheila Figel Dwyer, Lingqiu Gao, Irwin H. Gelman

Department of Cancer Genetics, Roswell Park Cancer Institute, USA.

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License. See for full terms and conditions.
Dwyer SF, Gao L, Gelman IH. Identification of Novel Focal Adhesion Kinase Substrates: Role for FAK in NFκB Signaling. Int J Biol Sci 2015; 11(4):404-410. doi:10.7150/ijbs.10273. Available from

File import instruction


Focal adhesion kinase (FAK) is a major signaling molecule which functions downstream of integrins or in conjunction with mitogenic signaling pathways. FAK is overexpressed and/or activated in many types of human tumors, in which it promotes cell adhesion, survival, migration and invasion. In addition to FAK's ability to regulate signaling through its scaffolding activities, FAK encodes an intrinsic kinase activity. Although some FAK substrates have been identified, a more comprehensive analysis of substrates is lacking. In this study, we use a protein microarray to screen the human proteome for FAK substrates. We confirm that several of the proteins identified are bona fide in vitro FAK substrates, including several factors which are known to regulate the NFκB pathway. Finally, we identify a role for FAK's kinase activity in both canonical and non-canonical NFκB signaling. Our screen therefore represents the first high throughput screen for FAK substrates and provides the basis for future in-depth analysis of the role of FAK's kinase activity in the processes of tumorigenesis.

Keywords: FAK, substrates, phosphotyrosine, kinase, NFκB, IKKα.