Focal adhesion kinase: in command and control of cell motility

By S. Mitra, Daniel A. Hanson, D. Schlaepfer. Nature reviews. Molecular cell biology, 2005

2,622 citations recorded by the source corpus.

Subfields: Cell Biology, Immunology and Allergy, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6ba2b63cb8409a242454723994e0b23de5cf6494

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Citations in the corpus

Cellular functions of FAK kinases: insight into molecular mechanisms and novel functions (2010, background): “FAK responds to extracellular stimuli, including signals from the extracellular matrix (ECM), and regulates cellular processes such as proliferation and cell migration (Mitra et al., 2005).”
Integrin signalling at a glance (2009, background): “…molecules to be identified was focal adhesion kinase (FAK), which acts as a phosphorylation-regulated signalling scaffold and is important for adhesion turnover, Rho-family GTPase activation, cell migration and cross-talk between growth-factor signalling and integrins (Mitra et al., 2005).”
The role of focal-adhesion kinase in cancer — a new therapeutic opportunity (2005, background): “This has been reviewed thoroughly in other articles, (for example, see Ref”
Matrix density-induced mechanoregulation of breast cell phenotype, signaling, and gene expression through a FAK-ERK linkage (2009, neutral): “…force between the cell and its microenvironment, and operate as a scaffolding node from which multiple signaling cascades emanate to regulate cell proliferation, survival, and migration (Burridge & Chrzanowska-Wodnicka, 1996; Geiger et al., 2001; Mitra et al., 2005; Playford & Schaller, 2004).”
Physics of adherent cells (2013, background): “Moreover, many signaling molecules responsible for cell migration, differentiation and fate are localized to focal adhesions, 19 most prominently the focal adhesion kinase, FAK, which is known to be important in many types of cancer (Mitra et al., 2005).”
Integrins in angiogenesis and lymphangiogenesis (2008, background): “Focal adhesion complexes are composed of integrins, protein kinases — such as focal adhesion kinase (FAK, also known as PTK2 ) and SRC — adaptor proteins such as Shc, signalling intermediates such as Rho family GTPases, actin-binding cytoskeletal proteins such as talin , α-actinin, paxillin , t”
Focal adhesion kinase and its signaling pathways in cell migration and angiogenesis (2010, background): “The activated PI3K could stimulate cell migration through its downstream effector Rac, which is a key regulator of cortical actin and lamellipodia in cell migration [60].”
Diffuse glioma growth: a guerilla war (2007, background): “cellular events such as proliferation, migration, survival, and apoptosis [117].”
Sense and stretchability: the role of titin and titin-associated proteins in myocardial stress-sensing and mechanical dysfunction. (2007, background): “linked kinase (ILK), Src-tyrosine kinase, zyxin, paxillin, protein-kinase-Cε, and members of the Rho-family GTPases (Samarel, 2005; Brancaccio et al., 2006; Mitra et al., 2005).”
Exploration of tumor-suppressive microRNAs silenced by DNA hypermethylation in oral cancer. (2008, background): “NCOA2/TIF2, a member of the p160 family of coactivators, and PTK2/FAK, a member of cytoplasmic nonreceptor protein tyrosine kinases, have been described to be associated with human cancer development (42, 43).”
FAK phosphorylation sites mapped by mass spectrometry (2005, background): “The protein tyrosine kinase, focal adhesion kinase (FAK), is a central regulator of integrin-mediated signaling ( Mitra et al., 2005; Parsons, 2003; Schlaepfer and Mitra, 2004).”
Extracellular matrix and cell signalling: the dynamic cooperation of integrin, proteoglycan and growth factor receptor. (2011, background): “The scaffolding interactions of integrins to the actin cytoskeleton involve actin polymerising and actin linking molecules, whose interactions regulate, and are regulated by, the associated adhesion signalling molecules (Mitra et al. 2005).”
Mechanics, malignancy, and metastasis: The force journey of a tumor cell (2009, background): “FAK is a nonreceptor tyrosine kinase that is widely overexpressed and activated in tumor cells [139–142].”