ABSTRACT
Monomeric actin (G-actin) polymerizes spontaneously into helical filaments in the presence of inorganic salts. The slowest, rate-limiting step of the polymerization process is formation of actin trimers, the smallest oligomers that serve as nuclei for fast filament growth (filament elongation) by monomer addition at the filament ends. In low ionic-strength solutions, actin can be polymerized by myosin subfragment-1 (S1). In early works it has been suggested that G-actin-S1 1:1 complexes (GS) assemble into filaments according to the nucleation-filament elongation scheme. Subsequent studies indicated that one S1 molecule can bind two actin monomers, and that oligomerization of the initial complexes is a fast reaction. This has led to suggest an alternative mechanism, with a ternary G(2)S complex and its oligomers being predominant intermediates of S1-induced assembly of G-actin into filaments. We used dynamic light scattering to analyze the initial steps of S1-induced polymerization of actin. Our results suggest formation of GS complexes and their oligomers in the presence of S1 equimolar to or in excess over actin. We confirm formation of G(2)S complexes as intermediates of S1-induced polymerization in the presence of actin in excess over S1.
Subject(s)
Actins/chemistry , Actins/metabolism , Myosin Subfragments/chemistry , Myosin Subfragments/metabolism , Animals , Particle Size , Rats , Spectrum AnalysisABSTRACT
Ultrasonographic examinations were carried out in 174 patients with various types of hyperlipoproteinaemia, determining the incidence of the features of liver steatosis. In the group of 77 patients with hypercholesterolaemia (TCH > 200 mg%) the features of liver steatosis occurred in 13 cases (16.9%). In 90 patients with mixed hyperlipidaemia (TCH > 200 mg%, TG > 2.3 mmol/l) the features of liver steatosis were found in 50% of cases. Both in the groups of patients with hypercholesterolaemia and with mixed HLP, the patients with liver steatosis had significantly higher body mass index. In the group of patients with hypercholesterolaemia (without and with the features of liver steatosis) no differences were found in the concentrations of total cholesterol (TCH), triglycerides (TG) and high density lipoprotein fraction (HDL). In the patients with mixed HLP and the features of liver steatosis in USG examination, the mean serum triglyceride concentration was 6.2 mmol/l and was almost twice higher than that in the group without steatosis. The serum HDL concentration in the patients with mixed HLP was 39.2 mg% and was significantly lower than that in the patients with the same type of lipid concentration disturbances but without liver steatosis (48.2 mg%). The total serum cholesterol concentration was not differing significantly between the patients with liver steatosis and those without this pathological condition.
