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In the noncanonical context, β-catenin functions as a component of membrane adhesion complexes.
DOI: http://dx.doi.org/10.7554/eLife.02372.021 Vertebrate tendons consist of a complex network of collagen-rich fibrils, which interact with other ECM proteins and membrane adhesion complexes on the surfaces of muscle cells to form attachments strong enough to bear contractile forces (Ros et al., 1995).
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These include proteins of the basement membranes and cell-cell adhesion complexes.
Enhanced cell adhesion by heparanase may be due to binding and activation of plasma membrane proteins such as syndecans, a class of trans-membrane HSPGs shown to modulate adhesion complexes [30], [31], [34].
We observed in both galectin-1 stable and galectin-1 transient knockdown cells a loss of integrin-β1 on the cell membrane at points of focal adhesion complexes coincident with an increase in intracellular levels of integrin-β1.
To develop metastasis, breast cancer cells need, among other steps, to break their intercellular adhesion complexes and basement membrane to acquire motility to invade adjacent tissues [ 1].
Myosin VI is crucial for border cell migration and since it exists in a complex with the adhesion proteins E-cadherin and β-catenin it could by binding to stationary adhesion complexes in the membrane develop a protrusive force by pushing the actin filaments outwards thus moving the cell forwards [65].
In response to specific chemoattractant signals, such as ECMs and growth factors, protrusions are formed at the leading edge by polymerization of actin filaments towards the cell plasma membrane, following the formation of focal adhesion complexes where activated integrins render the recruitment and activation of FAK [ 39, 40].
Myosin motor domain activity and the ability to bind to actin are likely to be important for the processes that require coordination of membrane deformation with actin filament recruitment, including cell shape changes, endocytosis, assembly of cell adhesion complexes and regulation of membrane tension.
Treatment with VEGF-C (100 ng/mL) up to 12 h led to the shift of the actin fibers toward the edge of the membrane, in association with the formation of specialized membrane structures like filopodia, pseudopodia and focal adhesion complexes (Fig. 1D).
Integrin-based adhesion complexes consist of membrane-cytoskeletal and signaling proteins, such as vinculin, which acts to couple integrin receptors to actin filaments [ 38, 39], talin, which induces integrin activation [ 40- 42] and focal adhesion kinase (FAK), which phosphorylates various targets and regulates dynamic adhesion turnover to stimulate growth cone migration [ 25, 43, 44].
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