FAK (focal adhesion kinase; PTK2) is a non-receptor cytoplasmic tyrosine kinase recruited to integrin-based focal adhesions at the cell membrane. Paxillin is a scaffold protein at the same adhesion complexes that binds FAK, vinculin and additional cytoskeletal partners.
Together, the FAK-paxillin axis couples integrin engagement with the extracellular matrix to cytoskeletal reorganisation, focal-adhesion turnover and directed cell migration. It is a central regulator of fibroblast, endothelial and epithelial motility during tissue repair.
In BPC-157 research, work by Chang and colleagues reports that BPC-157 promotes tendon fibroblast outgrowth and migration through the FAK-paxillin pathway.
