Identifying the targets of the amplifying pathway for insulin secretion in pancreatic beta-cells by kinetic modeling of granule exocytosis.

A kinetic model for insulin secretion in pancreatic beta-cells is adapted from a model for fast exocytosis in chromaffin cells. The fusion of primed granules with the plasma membrane is assumed to occur only in the "microdomain" near voltage-sensitive L-type Ca(2+)-channels, where [Ca(2+)] can reach micromolar levels. In contrast, resupply and priming of granules are assumed to depend on the cytosolic [Ca(2+)].

Ca2+ and ionic strength dependencies of S1-ADP binding to actin-tropomyosin-troponin: regulatory implications.

Skeletal and cardiac muscle contraction are inhibited by the actin-associated complex of tropomyosin-troponin. Binding of Ca(2+) to troponin or binding of ATP-free myosin to actin reverses this inhibition. Ca(2+) and ATP-free myosin stabilize different tropomyosin-actin structural arrangements.

Theoretical studies on competitive binding of caldesmon and myosin S1 to actin: prediction of apparent cooperativity in equilibrium and slow-down in kinetics of S1 binding by caldesmon.

Several laboratories have reported cooperative binding of S1 to actin in the presence of caldesmon. This cooperative binding has been interpreted with a model similar to that proposed for the binding of S1 to regulated actins in which the binding affinity of S1 is controlled by the position of the tropomyosin filaments. In a recent paper [Sen, A.

Fluctuations and randomness of movement of the bead powered by a single kinesin molecule in a force-clamped motility assay: Monte Carlo simulations.

The motility assay of K. Visscher, M. J.