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

A ubiquitin E3 ligase localizes to focal adhesions at the front of migrating human cells where it regulates cytoskeletal dynamics by targeting a focal adhesion protein.

Analysis of knockout and knockdown melanoma cells and TCGA melanoma data shows that the microphthalmia-associated transcription factor (MITF) is a major repressor of extracellular matrix (ECM) and focal adhesion genes.

Calcium influx stimulates formation of ER/plasma membrane contacts adjacent to focal adhesions, and lipid transfer at these sites is required for adhesion disassembly during cell migration.

In the cytosol, the proteins constituting cell-matrix adhesion sites form multi-protein building blocks which enter and leave these sites unaltered, thereby contributing to their rapid and correct self-assembly.

A novel two-step model for integrin activation primed by Cas during cell migration and spreading on multiple extracellular matrix ligands.

Cells control the spatial organization and signaling of TGFβ receptors at focal adhesions via a mechanically regulated mechanism to integrate biochemical and physical cues.

Ambra1 is a Src "spatial rheostat".

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.

Depletion of VAPA in cancer cells induces defects in actin organization, adhesion dynamics and cell migration, together with a perturbation of phosphoinositide levels at the plasma membrane and a lack of anchoring of ER-PM contact sites to focal adhesions.