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Cell surface (cortical) actin remodeling is a cyclic (9-step) process where each step is directly responsive to a cell signaling mechanism. Over the course of the cycle, actin begins as a monomer, elongates into a polymer with the help of attached actin-binding-proteins, and disassembles back into a monomer so the remodeling cycle may commence again.
In addition to actin polymerization, microtubules may also play an important role in cell migration where the formation of lamellipodia is involved. One experiment showed that although microtubules are not required for actin polymerization to create lamellipodial extensions, they are needed in order to afford cellular movement. [15]
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Actin plays a role in the formation of new spines as well as stabilizing spine volume increase. [1] The changes that actin brings about lead to the formation of new synapses as well as increased cell communication. Actin remodeling consists of the dynamic changes in actin polymerization that underlie the morphological changes at the neural synapse.
Many actin-related molecules create a free barbed end for polymerization by uncapping or severing pre-existing filaments and using these as actin nucleation cores. However, the Arp2/3 complex stimulates actin polymerization by creating a new nucleation core. Actin nucleation is an initial step in the formation of an actin filament.
The following steps describe one force-generating cycle of an actoclampin molecular motor: The polymerization cofactor profilin and the ATP·actin combine to form a profilin-ATP-actin complex that then binds to the end-tracking unit; The cofactor and monomer are transferred to the barbed-end of an actin already clamped filament
(Single white dots represent monomers and black chains represent oligomers and polymers) [1] Comparison of molecular weight vs conversion plot between step-growth and living chain-growth polymerization. In polymer chemistry, step-growth polymerization refers to a type of polymerization mechanism in which bi-functional or multifunctional ...
Actin polymerization can further be regulated by profilin and cofilin. [6] Cofilin functions by binding to ADP-actin on the negative end of the filament, destabilizing it, and inducing depolymerization. Profilin induces ATP binding to G-actin so that it can be incorporated onto the positive end of the filament.