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Cell adhesion is the process by which cells form contacts with each other or with their substratum through specialized protein complexes. Intercellular adhesion can be mediated by adherens junctions, tight junctions and desmosomes, whereas cells can interact with extracellular matrix molecules through focal adhesions.
The mechanisms controlling the formation of cellular adhesions are not fully understood. Here, the authors use single molecule tracking and super-resolution imaging to show that the actin cytoskeleton regulates integrin diffusion in the developing Drosophila embryo.
Integrin receptors connect cells to the extracellular matrix, mediating cell interactions, adhesion and signalling. This Review discusses integrin function in cell migration, including integrin activation, integrin-based adhesion types and their roles in cancer cell dissemination.
Phagocytosis is regulated by the mechanical properties of both the phagocyte and its cargo. Here, the authors show that macrophages employ β2 integrins to sense the rigidity of phagocytic cargo and then mount the appropriate form of engulfment.
In this Tools of the Trade article, Isomursu (Ivaska lab) describes a new method for dynamic micropatterning, which enables investigation of cell adhesion and migration on substrates that mimic different extracellular matrix environments.
Recently published in Nature, Fan et al. demonstrate that accumulation of advanced glycation end-products in the extracellular matrix of the liver increases viscoelasticity to promote hepatocellular carcinoma growth, independent of stiffness.
Cellâcell adhesions are inevitably exposed to mechanical forces. A landmark paper by Yonemura et al. identified how tension alters molecular function of the cadherin adhesion apparatus. Its legacy lies in the many on-going efforts to understand how mechanical force is used in cellâcell communication.
Effective pharmacological treatment options for abdominal aortic aneurysm (AAA) are missing. A study by Zhang et al. suggests that targeting the thrombo-inflammatory activity of platelets by blocking the intracellular accumulation of ceramides might limit AAA progression while not affecting hemostatic platelet function.