4.4 Actin Filament Nucleation and Elongation

摘要: The spontaneous polymerization of actin filaments is kinetically unfavorable because the instability intermediates (small oligomers), and it additionally inhibited in cells by actions monomer-binding proteins such as profilin thymosin-β4. Eukaryotic various pathogens use nucleation elongation factors to initiate promote polymer a localized regulated manner. Filament nucleators include Arp2/3 complex its large family promoting factors, formins, Spire, cordon-bleu (Cobl), leiomodin (Lmod), adenomatous polyposis coli (APC), Vibrio VopL/VopF, Chlamydia translocated recruiting phosphoprotein (TARP), Rickettsia Sca2. These molecules work different mechanisms, but they all share ability bind two or more subunits stabilize nucleus. abundance filament mechanisms correlates with diversity functions which these play cells, pathways are regulated. So far, formins only known class also stimulate processive barbed end elongation. By contrast, "enable/vasodilator stimulated (Ena/VASP)" function dedicated no role nucleation.