Just Science week has been fun, reading four recent journal articles on focal adhesion kinase (FAK). It has helped me refresh myself on FAK as I got back to writing fellowship applications – although it had the added effect of taking time away from said writing activities. So today I thought a recap was in order, and add an insightful review that came out a year and a half ago which is still very helpful.
An excerpt from Integrin signaling in directed cell migration, by Konstandinos Moissoglu and Martin Alexander Schwartz:
Because adhesions at the leading edge are continually being formed, while the trailing edge contains longer-lived stable adhesions that are continually being broken, polarization will tend to be maintained, resulting in persistent migration
in the same direction. One implication of these ideas is that integrin signals contribute to migration stimulated by growth factors and chemokines, thus blurring the distinction between chemotaxis and haptotaxis.
They’re talking about how this directionality in migration processes is maintained by spatially and temporally regulated dynamic structures called focal adhesions (so named because they are adhesion foci). The spatial dynamics are particularly interesting, as they are the result of multiple biochemical feedback signaling loops, including those of PI3K (and PTEN), Rac and Rho, and scaffolding proteins such as Paxillin, among others. And they’re all coordinated by FAK.
Now, the recap:
FAK, Pyk2, and p190RhoGEF in Cell Motility
FAK and Lamellipodia
Dissecting Molecular Interactions Between FAK and Paxillin
FAK and Phosphatidyl inositol in Cell Polarity
- Moissoglu K, Schwartz MA (2006) Biol Cell., 98(9):547-55. doi:10.1042/BC20060025
