The cell surface protein CD95 mediates neutrophil slow rolling and adhesion during inflammation.

Interactions between talin1 and a cortical scaffolding protein KANK1 control microtubule stabilization in the vicinity of focal adhesions.

Biochemical and cell biological data suggest a model of nascent integrin adhesion complex formation based on synergistic phase separation of pathways surrounding the focal adhesion kinase (FAK) and the adaptor protein p130Cas.

A numerical model of malaria parasite adhesion to an erythrocyte shows that the original egg-like shape of merozoites is more robust than other shapes in negotiating various physiological conditions during the alignment process upon erythrocyte invasion.

Cytosolic S100A8/A9 enhances Ca²⁺ availability at LFA-1 adhesion sites, facilitating neutrophil recruitment and extravasation by supporting proper integrin signaling and cytoskeletal rearrangement.

Planar cell polarity protein Celsr1 clusters into punctate assemblies through lateral cis-interactions to function as an organizer of intercellular Frizzled6 and Vangl2 asymmetry.

T cell progenitor homing into the thymus requires kindlin-3 to stabilize their adhesion to vascular integrin ligands when blood flow velocities and shear rates increase during development.

The bond-based adhesion model is a key step toward a realistic description of RBC-parasite interaction, which allows the investigation of more realistic scenarios and is relevant for other biological systems.

Tumor-induced myeloid-derived suppressor cells exert systemic suppression of adaptive immunity by limiting L-selectin-directed trafficking of T cells at vascular checkpoints in lymph nodes.

The interaction between activated αIIbβ3 on platelets and SLC44A2 on circulating neutrophils facilitates neutrophil capture and drives flow-dependent NETosis.