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Figure 11.5 Cofilin severs tethered actin filaments at nanomolar concentrations. The
severing of actin filaments by the cofilin mutant S3C was observed in the light microscope
and quantified in arbitrary units as described previously (Ichetovkin et al., 2002). The
severing is detected down to low nM concentrations for the S3C mutant as shown in the
figure and down to 9 nM for the wild-type cofilin (not shown) while the K 50 for severing by
wild-type cofilin is measured as mM in solution (Ichetovkin et al., 2002)
unpublished), and thus occurs after the peak of the early actin polymeriza-
tion transient has passed.
Conclusions
A summary cartoon of the pathways leading to actin polymerization in
carcinoma cells in response to the stimulation of EGF receptor is shown
in Figure 11.6. The early actin polymerization transient is indicated as
pathway 1 and involves cofilin activation by PLC-mediated PIP 2
hydrolysis to release a dephosphorylated population of cofilin from the
plasma membrane near activated EGF receptors (Wells et al., 1999). The
late actin polymerization transient is indicated as pathway 2 and involves
the relatively slow recruitment to the membrane of Rac/Cdc42 and WASp
family members leading to the activation of the Arp2/3 complex near to
the plasma membrane. Actin filaments polymerized proximal to the
receptor by pathway 1 could participate in the assembly of the F-actin
dependent EGF receptor
signalling complex (Heyden et al., 1997;
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