Integrins articles from across Nature Portfolio

Cells employ integrin-based adhesions with different molecular compositions to adhere to substrates. Here, the authors show that so-called “non-canonical” adhesions lacking focal adhesion components can convert to focal adhesions (and vice versa), through the selective exchange of components.

During alveologenesis myofibroblasts contractions at terminal sacs produce alveoli in the lungs. Here they show that endothelial cells promote myofibroblast-driven alveologenesis by forming basement membranes via Rap1-induced integrin β1 activation.

CD8⁺ T cell activation involves cooperation between the T cell receptor and the integrin LFA-1. Here authors show how LFA-1 nanoclusters participate in the calibration of TCR stimulation strength and activation of cytotoxic function in CD8⁺ T cells.

Here, the authors show how binding of talin and kindlin to the β-integrin cytoplasmic tail increases talin and decreases kindlin affinity toward it, providing insights into mechanisms of integrin activation.

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.

The fibrous geometry of extracellular matrices (ECMs) is believed to facilitate cell adhesion, but a mechanistic link is lacking. We uncover a type of integrin-mediated cell adhesion — ‘curved adhesion’ — driven by the fibrous geometry of the ECM. Curved adhesions are induced by membrane curvature, enabling cell adhesion to soft three-dimensional (3D) ECM fibres.

Nanofibre mimetic substrates reveal the presence of integrin nanoclusters bridged by unliganded receptors during early cell–matrix adhesion.

An intermediate affinity state of integrin α_IIBβ₃ has been identified to be a key player in platelet mechanosignalling.

Classical actin-dependent, integrin-mediated cell–matrix adhesions disassemble before mitotic rounding. Yet, to transmit positional information and facilitate daughter-cell separation, dividing cells maintain connections to the matrix. A previously unidentified class of actin-independent integrin adhesions may fulfil this task.

Single-cell force spectroscopy reveals rapid, biphasic integrin activation and reinforcement of cell–matrix bonds during the initial steps of fibroblast adhesion.