The DOI matches its Crossref record; 62 of the 62 references it cites were found in a registry or an index.
Cellular functions of FAK kinases: insight into molecular mechanisms and novel functions
Abstract
Focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2) are related tyrosine kinases that have important cellular functions, primarily through regulation of the cytoskeleton. Recent studies have identified multiple molecular mechanisms that regulate cytoskeletal responses, and have provided important and exciting insights into how FAK and Pyk2 control cellular processes such as cell migration. Equally exciting are reports of novel and originally unanticipated functions of these kinases, providing the groundwork for future avenues of investigation. This Commentary summarizes some of these recent discoveries that are relevant to the control of biological responses of the cell.
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Cites
Focal adhesion kinase: in command and control of cell motility.
Mitra, S. K., Hanson, D. A., & Schlaepfer, D. D. (2005) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1549 · Cited by 2,335
FAK–Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly
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Microtubule-induced focal adhesion disassembly is mediated by dynamin and focal adhesion kinase
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Focal adhesion kinase is involved in mechanosensing during fibroblast migration
Wang, H.-B., Dembo, M., Hanks, S. K., & Wang, Y.-L. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.201201198 · Cited by 502
Nuclear FAK Promotes Cell Proliferation and Survival through FERM-Enhanced p53 Degradation
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Focal adhesion kinase suppresses Rho activity to promote focal adhesion turnover
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Type Iγ phosphatidylinositol phosphate kinase targets and regulates focal adhesions
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Cell-Cycle Control by Physiological Matrix Elasticity and In Vivo Tissue Stiffening
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Cited by
FAK in cancer: mechanistic findings and clinical applications
Sulzmaier, F. J., Jean, C., & Schlaepfer, D. D. (2014) · Nature Reviews Cancer · doi:10.1038/nrc3792 · Cited by 1,381
FAK signaling in human cancer as a target for therapeutics
Lee, B. Y., Timpson, P., Horvath, L. G., & Daly, R. J. (2015) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2014.10.001 · Cited by 425
CB 1 and CB 2 Receptor Pharmacology
Howlett, A. C., & Abood, M. E. (2017) · Advances in Pharmacology · doi:10.1016/bs.apha.2017.03.007 · Cited by 375
Miyazaki, T., Futaki, S., Suemori, H., Taniguchi, Y., Yamada, M., Kawasaki, M., Hayashi, M., Kumagai, H., Nakatsuji, N., Sekiguchi, K., et al. (2012) · Nature Communications · doi:10.1038/ncomms2231 · Cited by 368
Addressing Kinase-Independent Functions of Fak via PROTAC-Mediated Degradation
Cromm, P. M., Samarasinghe, K. T. G., Hines, J., & Crews, C. M. (2018) · Journal of the American Chemical Society · doi:10.1021/jacs.8b08008 · Cited by 293
Metadata
- Authors
- Schaller, M. D.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2010-04-01
- Volume
- 123
- Issue
- 7
- Pages
- 1007-1013
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W2021705436
- Cited by
- 599
- References
- 62
- FWCI
- 30.97
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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