Sentence examples for central adhesion from inspiring English sources

Sun, Z. et al. Kank2 activates talin, reduces force transduction across integrins and induces central adhesion formation.

In addition, Kank proteins diminish the talin-actomyosin linkage, which curbs force transmission across integrins, leading to reduced integrin-ligand bond strength, slippage between integrin and ligand, central adhesion formation and sliding, and reduced cell migration speed.

It is assumed that the surface shear traction within the contact area is limited by Coulomb's friction law and the torsion angel was produced within the central adhesion zone as a rigid body.

Accordingly, p85β overexpression increased the number of central adhesions and reduced peripheral focal contacts and adhesion plaques (Fig. 3B).

The phenotypes induced by p85β expression in fibroblasts and BLM cells suggest that p85β induces maturation of peripheral contacts to central adhesions, as well as the development of F-actin-containing cell adhesions.

Under sufficiently high antigen stimulation, TCR clusters subsequently move inward to the center of the junction, forming the central supramolecular adhesion complex (c-SMAC).

Kank proteins accumulate at the lateral border of FAs, which we term the FA belt, and in central sliding adhesions, where they directly bind the talin rod domain through the Kank amino-terminal (KN) motif and induce talin and integrin activation.

GFP-tagged talin1 localised to peripheral FA as well as to more central fibrillar adhesions (FB) (Fig. 3A arrow), although a cytoplasmic pool of what may be auto-inhibited talin was located around the nucleus.

FAK activity is heavily influenced by growth factors and even subtle changes in FAK activity, or in the expression patterns of the proteins central to focal adhesions, will remodel focal adhesions to promote cell migration and invasion of cancer cells [ 51].

Although stress fibers (bundles of actin filaments) play a central role in adhesion, motility, and morphogenesis of eukaryotic cells, the mechanism of how these and other contractile actomyosin structures are controlled and redistributed in the cell is not well understood.

Col8−/− SMCs exhibited impairments in migration, and a strongly adhesive phenotype with prominent stress fibers, stable microtubules and pronounced central basal focal adhesions.