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Sink binding-maintained

Receiver wells pH 7.4 phosphate buffer containing 3% w/v bovine serum albumin (BSA) added to receiver wells (binding-maintained sink). [Pg.123]

Binding-maintained sink conditions The presence of serum proteins in the receiver wells, such as 3% w/v BSA, will bind the neutral compound once it crosses the membrane. [Pg.125]

ThepION Inc. method uses double-sink conditions, both ionization and binding maintained. [Pg.125]

In this chapter we use the term sink to mean any process that can significantly lower the concentration of the neutral form of the sample molecule in the acceptor compartment. Under the right conditions, the ionization and the binding sinks serve the same purpose as the physically maintained sink often used in Caco-2 measurements. We will develop several transport models to cover these chemical sink conditions. When both of the chemical sink conditions (ionization and binding) are imposed, we will use the term double sink in this chapter. [Pg.139]

Donor wells pH 6 and pH 7 (ionization-maintained sink), 5-10 mm bile acid, such as taurocholic acid or glycocholic acid to solubilize lipophilic molecules (binding-... [Pg.123]

Fig. 4 The lipid influx/efflux rheostat model maintains lipid uptake and export mechanisms in a balance. ATP synthase is regulated by apoA-I or apoE leading to enhanced conversion of ATP to ADP. The absence of apoA-I would lead to enhanced sinking in phagocytosis since actin can bind ATP, polymerize, and form F-actin which is essential for type 11 phagocytosis. Hence apoA-I could lead to increased influx. On the other hand, apoA-I binds to ABCAl leading to enhanced lipid efflux. Dysfunction of this equilibrium may lead to severe disturbances of cellular lipid traffic. This is obvious in Tangier disease patients where ABCAl is inoperative and apoA-/-dependent cholesterol is absent. Cholesterol influx, however, is enhanced due to apoA-Z-dependent stimulation of ATP synthase B leading to cholesteryl ester formation and enhanced foam cell formation... Fig. 4 The lipid influx/efflux rheostat model maintains lipid uptake and export mechanisms in a balance. ATP synthase is regulated by apoA-I or apoE leading to enhanced conversion of ATP to ADP. The absence of apoA-I would lead to enhanced sinking in phagocytosis since actin can bind ATP, polymerize, and form F-actin which is essential for type 11 phagocytosis. Hence apoA-I could lead to increased influx. On the other hand, apoA-I binds to ABCAl leading to enhanced lipid efflux. Dysfunction of this equilibrium may lead to severe disturbances of cellular lipid traffic. This is obvious in Tangier disease patients where ABCAl is inoperative and apoA-/-dependent cholesterol is absent. Cholesterol influx, however, is enhanced due to apoA-Z-dependent stimulation of ATP synthase B leading to cholesteryl ester formation and enhanced foam cell formation...

See other pages where Sink binding-maintained is mentioned: [Pg.139]    [Pg.90]    [Pg.267]    [Pg.2556]    [Pg.718]    [Pg.145]    [Pg.60]    [Pg.206]    [Pg.160]    [Pg.2555]    [Pg.337]    [Pg.195]    [Pg.90]    [Pg.355]   
See also in sourсe #XX -- [ Pg.125 ]




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