Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Model mechanism, phagocytosis

Actin and tubulin are two important cellular components that are involved in cell shape and movement. Actin is present in all mammalian cells and is involved in cellular transport and phagocytosis (eating of extracellular materials), provides rigidity to cell membranes, and when bonded to tropomyosin and troponin, forms the thin filaments of muscle. Thbulin is the subunit from which microtubules are self-assembled. Microtubules are most commonly known for their role in cell division. The mechanisms of self-assembly of these macromolecules have been well studied and are important models of biological assembly processes. Below we examine each of these processes. [Pg.159]

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...
Herant, M., Heinrich, V. and Dembo, M. (2005) Mechanics of neutrophil phagocytosis experiments and quantitative models. Journal of Cell Science, 119, 1903-13. [Pg.354]


See other pages where Model mechanism, phagocytosis is mentioned: [Pg.310]    [Pg.419]    [Pg.169]    [Pg.271]    [Pg.105]    [Pg.454]    [Pg.421]    [Pg.402]    [Pg.681]    [Pg.120]    [Pg.681]    [Pg.1193]    [Pg.239]    [Pg.321]    [Pg.134]    [Pg.13]    [Pg.536]    [Pg.2001]    [Pg.372]    [Pg.137]    [Pg.175]    [Pg.120]    [Pg.140]    [Pg.1361]    [Pg.1361]    [Pg.561]    [Pg.777]    [Pg.15]    [Pg.885]    [Pg.332]    [Pg.128]    [Pg.580]    [Pg.203]   


SEARCH



Mechanical models

Mechanics Model

Mechanics Modeling

Mechanism model

Mechanisms modeling

© 2024 chempedia.info