ATPases mechanisms

Walmsley AR, T Zhou, Ml Boirges-Walmsley, BP Rosen (1999) The ATPase mechanism of ArsA, the catalytic subunit of the arsenite pump. J Biol Chem 274 16153-16161. 

Song, Y. H., Marx, A., Muller, J., Woehlke, G., Schliwa, M., Krebs, A., Hoenger, A., and Mandelkow, E. (2001). Structure of a fast kinesin Implications for ATPase mechanism and interactions with microtubules. EMBO J. 20, 6213-6225. 

F-ATPase is a reversible enzyme that can work in the direction of proton gradient-driven ATP synthesis and in the direction of ATP hydrolysis-driven proton pumping. Reversibility has recently been shown by elegantly turning the rotor in the F-ATPase mechanically in the direction of ATP synthesis. When ADP and inorganic phosphate were present during the forced rotation, ATP was synthesized and released from the enzyme (Itoh et al, 2004). This means that the complex contains two molecular motors the F, which is an ATP hydrolysis-driven motor, and the F0, which is a... 

Marston SB, Taylor EW (1980) Comparison of the myosin and actomyosin ATPase mechanisms of the four types of vertebrate muscles. J Mol Biol 139 573600 Matsu-ura M, Ikebe M (1995) Requirement of the two -headed structure for the phosphorylation dependent regulation of smooth muscle myosin. FEBS Lett 363 246250... 

Trentham, D. R., Eccleston, J. F. Bagshaw, C. R. (1976). Kinetic analysis of ATPase mechanisms. Quarterly Reviews of Biophysics, 9, 217-81. 

Ishijima A, Kojima H, Funatsu T, Tokunaga M, Higuchi H, Tanaka H and Yanagida T 1998 Simultaneous observation of individual ATPase and mechanical events by a single myosin molcule during interaction with actin Ce//92 161-71... 

Succinimides. Ethosuximide [77-67-8] C2H22NO2 (41) and the related succinknide, methsuximide [77-41-8] C22H23NO2 (42) are used in absence seizure treatment. Like the other anticonvulsants discussed, the mechanism of action of the succinirnides is unclear. Effects on T-type calcium channels and -ATPase activity have been reported (20). Ethosuximide has significant CNS and gastrointestinal (GI) side effect HabiUties (13). 

Contraction of muscle follows an increase of Ca " in the muscle cell as a result of nerve stimulation. This initiates processes which cause the proteins myosin and actin to be drawn together making the cell shorter and thicker. The return of the Ca " to its storage site, the sarcoplasmic reticulum, by an active pump mechanism allows the contracted muscle to relax (27). Calcium ion, also a factor in the release of acetylcholine on stimulation of nerve cells, influences the permeabiUty of cell membranes activates enzymes, such as adenosine triphosphatase (ATPase), Hpase, and some proteolytic enzymes and facihtates intestinal absorption of vitamin B 2 [68-19-9] (28). 

A minimal mechanism for Na, K -ATPase postulates that the enzyme cycles between two principal conformations, denoted Ej and Eg (Figure 10.11). El has a high affinity for Na and ATP and is rapidly phosphorylated in the presence of Mg to form Ei-P, a state which contains three oeeluded Na ions (occluded in the sense that they are tightly bound and not easily dissociated from the enzyme in this conformation). A conformation change yields Eg-P, a form of the enzyme with relatively low affinity for Na, but a high affinity for K. This state presumably releases 3 Na ions and binds 2 ions on the outside of the cell. Dephosphorylation leaves EgKg, a form of the enzyme with two... 

FIGURE 10.11 A mechanism for Na, K -ATPase. The model assumes two principal conformations, Ei and E9. Binding of Na ions to Ei is followed by phosphorylation and release of ADP. Na ions are transported and released and ions are bound before dephosphorylation of the enzyme. Transport and release of ions complete the cycle. 

FIGURE 10.15 A mechanism for Ca -ATPase from sarcoplasmic reticulum. Note the similarity to the mechanism of Na, K -ATPase (see also Figure 10.11). ( Out here represents the cytosol In represents the lumen of the SR.)... 

The discovery of the antiulcer activity of H2 antihistamine antagonists has revolutionized the treatment of that disease. A benzimidazole. Omeprazole (55), inhibits gastric secretion and subsequent ulcer formation by a quite different mechanism. Studies at the molecular level suggest that this compound inhibits K /H dependent ATPase and consequently shuts down the proton pumping action of this enzyme system. 

Additional cellular events linked to the activity of blood pressure regulating substances involve membrane sodium transport mechanisms Na+/K.+ ATPase Na+fLi countertransport Na+ -H exchange Na+-Ca2+ exchange Na+-K+ 2C1 transport passive Na+ transport potassium channels cell volume and intracellular pH changes and calcium channels. 

Proton Pump Inhibitors and Acid Pump Antagonists. Figure 2 Chemical mechanism of irreversible PPIs. PPIs are accumulated in acidic lumen and converted to active sulfenic acid and/or sulfenamide by acid catalysis. These active forms bind to extracytoplasmic cysteines of the gastric H.K-ATPase [3]. 

The structure and mechanism of the sarcoplasmic reticulum Ca2+-ATPase a bioinorganic perspective. E. M. Stephens andC. M. Grisham, Adv. Inorg. Biochem., 1982, 4, 263-288 (151). 

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