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Membrane ruffling

C1C-6 is a late endosomal chloride transporter. Its disruption in mice led to lysosomal storage disease. C1C-7 is expressed in late endosomes and lysosomes. It needs Ostml as (3-subunit [3]. The disruption of either C1C-7 or Ostml in mice and man leads to severe osteopetrosis, retinal degeneration, and a severe lysosomal storage disease. ClC-7/Ostml is highly expressed in osteoclasts. In these cells, it is inserted together with the proton pump into the specialized plasma membrane ( ruffled border ) that faces the reabsorption lacuna. Osteoclasts are still present in C1C-7 knockout... [Pg.372]

Franck, Z., Footer, M., Bretscher, A. (1990). Microinjection of villin in cultured cells induces rapid and long-lasting changes in cell morphology but does not inhibit cytokinesis, cell motility or membrane ruffling. J. Cell Biol. Ill, 2475-2485. [Pg.103]

Ridley, A.J., Paterson, H.F., Johnston, C.L., Diekermann, D., Hall, A. (1992). The small GTP-binding protein rac regulates growth factor-induced membrane ruffling. Cell, 70,401-410. [Pg.105]

In Fig. 9.4, the results are shown of an experiment using a double (annexinA4-EYFP+ annexinA4-mCherry) transfected cell immediately after addition of the calcium ionophore ionomycin (top) and 5 min after application of ionomycin (bottom). Clearly visible is the diffuse localization of annexin A4 before relocation and the more structured localization (into membrane ruffles and filopodia) after relocation. More importantly, the EYFP fluorescence lifetime is quenched from 2.9 ns before translocation to... [Pg.417]

Figure 13.9 represents the TEM image of LDH particles and their cellular internalization. As expected, LDH particles are internalized by endocytosis. Figure 13.9(A) shows the cellular uptake process of LDHs after 3h of treatment, and demonstrates a successive entry of LDH by endocytosis first the LDH particles were located around the cell membrane due to their positive charge ( ), then they migrate to the membrane ruffles which are considered as endocytic bodies ( ), finally the coated intracellular vesicles were formed as early endosomes ( ). Figure 13.9(B)... Figure 13.9 represents the TEM image of LDH particles and their cellular internalization. As expected, LDH particles are internalized by endocytosis. Figure 13.9(A) shows the cellular uptake process of LDHs after 3h of treatment, and demonstrates a successive entry of LDH by endocytosis first the LDH particles were located around the cell membrane due to their positive charge ( ), then they migrate to the membrane ruffles which are considered as endocytic bodies ( ), finally the coated intracellular vesicles were formed as early endosomes ( ). Figure 13.9(B)...
Fig. 13.9 Transmission electron microscopic data ofendocytosis. Saos-2 cell was treated with LDH and after 1 h the cell was fixed and subjected to TEM measurement. (A) successive internalization of LDH via endocytosis access of LDH around plasma membrane, formation of membrane ruffles and interaction... Fig. 13.9 Transmission electron microscopic data ofendocytosis. Saos-2 cell was treated with LDH and after 1 h the cell was fixed and subjected to TEM measurement. (A) successive internalization of LDH via endocytosis access of LDH around plasma membrane, formation of membrane ruffles and interaction...
After membrane ruffling and formation of the so-called pseudopodia, the material is engulfed by the cell and is further transported to vesicles (phagosomes/macropinosomes) that have the ability to become acidified. These vesicles fuse rapidly with late endosomes and/or lysosomes, exposing their contents to the hydrophilic enzymes. [Pg.344]

Cell migration involves transient formation of membrane protmsions (lamellipodia, cell membrane ruffles) at the leading edge of the cell that are thought to require rapid local changes in ion fluxes and cell volume, probably accompanied by rapid transmembrane water movement (Condeelis 1993 Lauffenburger and Horwitz 1996). If transmembrane water movement is a fundamental determinant of cell motility, then a different water channel... [Pg.50]

Fujita, R., Ma, Y., and Ueda, H. (2008). Lysophosphatidic acid-induced membrane ruffling and brain-derived neurotrophic factor gene expression are mediated by ATP release in primary microglia. J. Neurochem. 107, 152—160. [Pg.187]

Joyce, P.L., and Cox, A.D. (2003). Racl and Rac3 are targets for geranylgeranyltransfer-ase I inhibitor-mediated inhibition of signaling, transformation, and membrane ruffling. Cancer Res 63 7959-7967. [Pg.156]

Rac proteins (Racl,2), which are also members of the Rho subfamily, are involved in membrane ruffling and lamellipodia formation induced by growth factors (Ridley et al., 1992 Hall, 1994), and it has also been suggested that they are important for Ras-induced transformation (Qiu et al., 1995). Moreover, Rac proteins control NADPH oxidase (Abo et al., 1991 Bokoch, 1994), and may have a role in phospholipase A2 regulation (Peppelenbosch et al., 1995). Cdc42, another member of the Rho family, which occurs in at least two iso-... [Pg.65]


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