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Curr Opin Cell Biol. 2017 Apr;45:24-30. doi: 10.1016/j.ceb.2017.01.003. Epub 2017 Feb 16.

Focal adhesion kinase signaling in unexpected places.

Author information

1
Biomedical Sciences Graduate Program, University of California, San Diego, CA, United States; Moores Cancer Center, Department of Reproductive Medicine, 3855 Health Sciences Drive, MC 0983, La Jolla, CA 92093-0983, United States.
2
Biomedical Sciences Graduate Program, University of California, San Diego, CA, United States; Moores Cancer Center, Department of Reproductive Medicine, 3855 Health Sciences Drive, MC 0983, La Jolla, CA 92093-0983, United States. Electronic address: dschlaepfer@ucsd.edu.

Abstract

Focal adhesion kinase (FAK) is a cytoplasmic protein-tyrosine kinase first identified at extracellular matrix and integrin receptor cell adhesion sites and is a key regulator of cell movement. FAK is activated by a variety of stimuli. Herein, we discuss advances in conformational-associated FAK activation and dimerization mechanisms. Additionally, new roles have emerged for FAK signaling at cell adhesions, adherens junctions, endosomes, and the nucleus. In light of these new findings, we review how FAK activation at these sites is connected to the regulation of integrin recycling-activation, vascular permeability, cell survival, and transcriptional regulation, respectively. Studies uncovering FAK signaling connections in unexpected places within cells have yielded important new regulatory insights in cell biology.

PMID:
28213315
PMCID:
PMC5482783
DOI:
10.1016/j.ceb.2017.01.003
[Indexed for MEDLINE]
Free PMC Article

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